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        <title>Experimental Cell Research via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Experimental Cell Research' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Experimental+Cell+Research&t=Experimental+Cell+Research&s=Search&f=source]]></link>
        <lastBuildDate>Tue, 07 Feb 2012 08:48:57 +0100</lastBuildDate>
        <item>
            <title>Dab2 is pivotal for endothelial cell migration by mediating VEGF expression in cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5623239&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22265793%26dopt%3DAbstract</link>
            <description>Authors: Cheong SM, Choi H, Hong BS, Gho YS, Han JK
    Abstract
    Although angiogenesis is crucial for tumor growth and metastasis, the molecular mechanisms controlling this process are not clearly understood. Here, we explore the role of Dab2 in tumor angiogenesis. We found that Dab2 is expressed in several cancer cells, including A549 lung cancer cells, but it is hardly detectable in SW480 colon cancer cells. Migration and Erk phosphorylation were enhanced in human umbilical vein endothelial cells (HUVECs) treated with the conditioned medium obtained from Dab2-overexpressing SW480 stable cells. In addition, vascular endothelial growth factor (VEGF) protein was strongly detected in conditioned medium derived from Dab2-overexpressing SW480 cells, and Erk phosphorylation enhanced by Dab2...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5623239</comments>
            <pubDate>Sat, 14 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Comparative analysis of stress responses of H9c2 rat cardiomyoblasts following treatment with doxorubicin and tBOOH.</title>
            <link>http://www.medworm.com/index.php?rid=5623238&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22265794%26dopt%3DAbstract</link>
            <description>Authors: Döhrmann M, Schorr A, Hülsenbeck J, Rasmussen TL, Issinger OG, Fritz G
    Abstract
    Cardiotoxicity is the major dose-limiting adverse effect of anthracyclines and is hypothesized to result from damage induced by reactive oxygen species (ROS) or inhibition of topoisomerase II. Here, we comparatively analyzed the effect of doxorubicin and the organic peroxide tertiary-butylhydroperoxide (tBOOH) on stress responses of rat cardiomyblast cells (H9c2). Moreover, we investigated the impact of serum factors and the novel prototypical protein kinase CK2 inhibitor resorufin on the sensentivity of H9c2 cells exposed to doxorubicin or tBOOH. Measuring cell viability by use of the WST assay as well as cell cycle progression and apoptotic death by FACS-based methods, we found that the sen...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5623238</comments>
            <pubDate>Fri, 13 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5623238</guid>        </item>
        <item>
            <title>Requirement of matrix metalloproteinase-1 for intestinal homeostasis in the adult Drosophila midgut.</title>
            <link>http://www.medworm.com/index.php?rid=5623237&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22265916%26dopt%3DAbstract</link>
            <description>Authors: Lee SH, Park JS, Kim YS, Chung HY, Yoo MA
    Abstract
    Stem cells are tightly regulated by both intrinsic and extrinsic signals as well as the extracellular matrix (ECM) for tissue homeostasis and regenerative capacity. Matrix metalloproteinases (MMPs), proteolytic enzymes, modulate the turnover of numerous substrates, including cytokine precursors, growth factors, and ECM molecules. However, the roles of MMPs in the regulation of adult stem cells are poorly understood. In the present study, we utilize the Drosophila midgut, which is an excellent model system for studying stem cell biology, to show that Mmp1 is involved in the regulation of intestinal stem cells (ISCs). The results showed that Mmp1 is expressed in the adult midgut and that its expression increases with age and...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5623237</comments>
            <pubDate>Thu, 12 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5623237</guid>        </item>
        <item>
            <title>Microvesicle and tunneling nanotube mediated intercellular transfer of g-protein coupled receptors in cell cultures.</title>
            <link>http://www.medworm.com/index.php?rid=5623236&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22266577%26dopt%3DAbstract</link>
            <description>Authors: Guescini M, Leo G, Genedani S, Carone C, Pederzoli F, Ciruela F, Guidolin D, Stocchi V, Mantuano M, Borroto-Escuela DO, Fuxe K, Agnati LF
    Abstract
    Recent evidence shows that cells exchange collections of signals via microvesicles (MVs) and tunneling nano-tubes (TNTs). In this paper we have investigated whether in cell cultures GPCRs can be transferred by means of MVs and TNTs from a source cell to target cells. Western blot, transmission electron microscopy and gene expression analyses demonstrate that A(2A) and D(2) receptors are present in released MVs. In order to further demonstrate the involvement of MVs in cell-to-cell communication we created two populations of cells (HEK293T and COS-7) transiently transfected with D(2)R-CFP or A(2A)R-YFP. These two types of cells w...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5623236</comments>
            <pubDate>Wed, 11 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Role of poly(ADP-ribose) glycohydrolase in the regulation of cell fate in response to benzo(a)pyrene.</title>
            <link>http://www.medworm.com/index.php?rid=5623235&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22266578%26dopt%3DAbstract</link>
            <description>Authors: Huang HY, Cai JF, Liu QC, Hu GH, Xia B, Mao JY, Wu DS, Liu JJ, Zhuang ZX
    Abstract
    Poly(ADP-ribosyl)ation is a crucial regulator of cell fate in response to genotoxic stress. Poly(ADP-ribosyl)ation plays important roles in multiple cellular processes, including DNA repair, chromosomal stability, chromatin function, apoptosis, and transcriptional regulation. Poly(ADP-ribose) (PAR) degradation is carried out mainly by poly(ADP-ribose) glycohydrolase (PARG) enzymes. Benzo(a)pyrene (BaP) is a known human carcinogen. Previous studies in our laboratory demonstrated that exposure to BaP caused a concentration-dependent DNA damage in human bronchial epithelial (16HBE) cells. The role of PARG in the regulation of DNA damage induced by BaP is still unclear. To gain insight into the f...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5623235</comments>
            <pubDate>Wed, 11 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Stage-specific embryonic antigen-4 identifies human dental pulp stem cells.</title>
            <link>http://www.medworm.com/index.php?rid=5623234&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22266579%26dopt%3DAbstract</link>
            <description>Authors: Kawanabe N, Murata S, Fukushima H, Ishihara Y, Yanagita T, Yanagita E, Ono M, Kurosaka H, Kamioka H, Itoh T, Kuboki T, Yamashiro T
    Abstract
    Embryonic stem cell-associated antigens are expressed in a variety of adult stem cells as well as embryonic stem cells. In the present study, we investigated whether stage-specific embryonic antigen (SSEA)-4 can be used to isolate dental pulp (DP) stem cells. DP cells showed plastic adherence, specific surface antigen expression, and multipotent differentiation potential, similar to mesenchymal stem cells (MSC). SSEA-4+ cells were found in cultured DP cells in vitro as well as in DP tissue in vivo. Flow cytometric analysis demonstrated that 45.5% of the DP cells were SSEA-4+. When the DP cells were cultured in the presence of all-trans...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5623234</comments>
            <pubDate>Wed, 11 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5623234</guid>        </item>
        <item>
            <title>RIM, Munc13, and Rab3A interplay in acrosomal exocytosis.</title>
            <link>http://www.medworm.com/index.php?rid=5602429&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22248876%26dopt%3DAbstract</link>
            <description>Authors: Bello OD, Zanetti MN, Mayorga LS, Michaut MA
    Abstract
    Exocytosis is a highly regulated, multistage process consisting of multiple functionally definable stages, including recruitment, targeting, tethering, priming, and docking of secretory vesicles with the plasma membrane, followed by calcium-triggered membrane fusion. The acrosome reaction of spermatozoa is a complex, calcium-dependent regulated exocytosis. Fusion at multiple sites between the outer acrosomal membrane and the cell membrane causes the release of the acrosomal contents and the loss of the membranes surrounding the acrosome. Not much is known about the molecules that mediate membrane docking in this particular fusion model. In neurons, the formation of the ternary RIM/Munc13/Rab3A complex has been suggested...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5602429</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5602429</guid>        </item>
        <item>
            <title>Protein kinase D1 stimulates proliferation and enhances tumorigenesis of MCF-7 human breast cancer cells through a MEK/ERK-dependent signaling pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5602434&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22245102%26dopt%3DAbstract</link>
            <description>Authors: Karam M, Legay C, Auclair C, Ricort JM
    Abstract
    Protein kinase D1, PKD1, is a novel serine/threonine kinase whose altered expression and dysregulation in many tumors as well as its activation by several mitogens suggest that this protein could regulate proliferation and tumorigenesis. Nevertheless, the precise signaling pathways used are still unclear and the potential direct role of PKD1 in tumor development and progression has not been yet investigated. In order to clarify the role of PKD1 in cell proliferation and tumorigenesis, we studied the effects of PKD1 overexpression in a human adenocarcinoma breast cancer cell line, MCF-7 cells. We demonstrated that overexpression of PKD1 specifically promotes MCF-7 cell proliferation through accelerating G0/G1 to S phase transi...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5602434</comments>
            <pubDate>Sun, 08 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5602434</guid>        </item>
        <item>
            <title>Fully functional global genome repair of (6-4) photoproducts and compromised transcription-coupled repair of cyclobutane pyrimidine dimers in condensed mitotic chromatin.</title>
            <link>http://www.medworm.com/index.php?rid=5602430&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22248875%26dopt%3DAbstract</link>
            <description>Authors: Komura JI, Ikehata H, Mori T, Ono T
    Abstract
    During mitosis, chromatin is highly condensed, and activities such as transcription and semiconservative replication do not occur. Consequently, the condensed condition of mitotic chromatin is assumed to inhibit DNA metabolism by impeding the access of DNA-transacting proteins. However, about 40years ago, several researchers observed unscheduled DNA synthesis in UV-irradiated mitotic chromosomes, suggesting the presence of excision repair. We re-examined this subject by directly measuring the removal of UV-induced DNA lesions by an ELISA and by a Southern-based technique in HeLa cells arrested at mitosis. We observed that the removal of (6-4) photoproducts from the overall genome in mitotic cells was as efficient as in interphas...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5602430</comments>
            <pubDate>Sun, 08 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5602430</guid>        </item>
        <item>
            <title>Arl5b is a Golgi-localised small G protein involved in the regulation of retrograde transport.</title>
            <link>http://www.medworm.com/index.php?rid=5602431&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22245584%26dopt%3DAbstract</link>
            <description>Authors: Houghton FJ, Bellingham SA, Hill AF, Bourges D, Ang DK, Gemetzis T, Gasnereau I, Gleeson PA
    Abstract
    Regulation of membrane transport is controlled by small G proteins, which include members of the Rab and Arf families. Whereas the role of the classic Arf family members are well characterized, many of the Arf-like proteins (Arls) remain poorly defined. Here we show that Arl5a and Arl5b are localised to the trans-Golgi in mammalian cells, and furthermore have identified a role for Arl5b in the regulation of retrograde membrane transport from endosomes to the trans-Golgi network (TGN). The constitutively active Arl5b (Q70L)-GFP mutant was localised efficiently to the Golgi in HeLa cells whereas the dominant-negative Arl5b (T30N)-GFP mutant was dispersed throughout the cytopl...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5602431</comments>
            <pubDate>Thu, 05 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5602431</guid>        </item>
        <item>
            <title>Fused in sarcoma (FUS) interacts with the cytolinker protein plectin: Implications for FUS subcellular localization and function.</title>
            <link>http://www.medworm.com/index.php?rid=5602436&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22240165%26dopt%3DAbstract</link>
            <description>Authors: Thomsen C, Udhane S, Runnberg R, Wiche G, Ståhlberg A, Aman P
    Abstract
    Fused in sarcoma (FUS) is a multifunctional protein involved in transcriptional control, pre-mRNA processing, RNA transport and translation. The domain structure of FUS reflects its functions in gene regulation and its ability to interact with other proteins, RNA and DNA. By use of a recombinant fragment of FUS in pull-down experiments followed by mass spectrometry analysis we have identified a novel interaction between the FUS N-terminal and the cytolinker plectin. An in situ proximity ligation assay confirmed that FUS-plectin interactions take place in the cytoplasm of cells. Furthermore, plectin deficient cells showed an altered subcellular localization of FUS and a deregulated expression of mRNAs b...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5602436</comments>
            <pubDate>Wed, 04 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5602436</guid>        </item>
        <item>
            <title>Role of Epac and protein kinase A in thyrotropin-induced gene expression in primary thyrocytes.</title>
            <link>http://www.medworm.com/index.php?rid=5602435&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22240166%26dopt%3DAbstract</link>
            <description>Authors: van Staveren WC, Beeckman S, Tomás G, Dom G, Hébrant A, Delys L, Vliem MJ, Trésallet C, Andry G, Franc B, Libert F, Dumont JE, Maenhaut C
    Abstract
    cAMP pathway activation by thyrotropin (TSH) induces differentiation and gene expression in thyrocytes. We investigated which partners of the cAMP cascade regulate gene expression modulations: protein kinase A and/or the exchange proteins directly activated by cAMP (Epac). Human primary cultured thyrocytes were analysed by microarrays after treatment with the adenylate cyclase activator forskolin, the protein kinase A (PKA) activator 6-MB-cAMP and the Epac-selective cAMP analog 8-pCPT-2'-O-Me-cAMP (007) alone or combined with 6-MB-cAMP. Profiles were compared to those of TSH. Cultures treated with the adenylate cyclase- or th...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5602435</comments>
            <pubDate>Wed, 04 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5602435</guid>        </item>
        <item>
            <title>Autophagy regulation in macrophages and neutrophils.</title>
            <link>http://www.medworm.com/index.php?rid=5602433&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22245582%26dopt%3DAbstract</link>
            <description>Authors: Mihalache CC, Simon HU
    Abstract
    Autophagy is a conserved proteolytic mechanism that degrades cytoplasmic material including cell organelles. Accumulating evidence exists that autophagy also plays a major role in immunity and inflammation. Specifically, it appears that autophagy protects against infections and inflammation. Here, we review recent work performed in macrophages and neutrophils, which both represent critical phagocytes in mammalians.
    PMID: 22245582 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5602433</comments>
            <pubDate>Wed, 04 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5602433</guid>        </item>
        <item>
            <title>Identification of new interacting partners of the shuttling protein ubinuclein (Ubn-1).</title>
            <link>http://www.medworm.com/index.php?rid=5602432&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22245583%26dopt%3DAbstract</link>
            <description>Authors: Lupo J, Conti A, Sueur C, Coly PA, Couté Y, Hunziker W, Burmeister WP, Germi R, Manet E, Gruffat H, Morand P, Boyer V
    Abstract
    We have previously characterized ubinuclein (Ubn-1) as a NACos (Nuclear and Adherent junction Complex components) protein which interacts with viral or cellular transcription factors and the tight junction (TJ) protein ZO-1. The purpose of the present study was to get more insights on the binding partners of Ubn-1, notably those present in the epithelial junctions. Using an in vivo assay of fluorescent protein-complementation assay (PCA), we demonstrated that the N-terminal domains of the Ubn-1 and ZO-1 proteins triggered a functional interaction inside the cell. Indeed, expression of both complementary fragments of venus fused to the N-terminal p...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5602432</comments>
            <pubDate>Wed, 04 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5602432</guid>        </item>
        <item>
            <title>Corneal stromal cells use both high- and low-contractility migration mechanisms in 3-D collagen matrices.</title>
            <link>http://www.medworm.com/index.php?rid=5602438&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22233682%26dopt%3DAbstract</link>
            <description>In this study, we investigated how culture conditions, ECM properties, and Rho kinase activity regulate the mechanics of keratocyte migration, using a nested collagen matrix model. Time-lapse imaging demonstrated that both serum and PDGF stimulate keratocyte migration into the outer matrix. Although the velocity of cell migration was similar, cells in serum were bipolar and induced significant matrix deformation during migration, whereas PDGF induced extension of branching dendritic processes with smaller, more localized force generation. These differences in cell-induced matrix reorganization were verified with a global matrix contraction assay and confocal reflection imaging, using both bovine and rat tail collagen. When constructs were detached from the substrate to lower the effective ...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5602438</comments>
            <pubDate>Mon, 02 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5602438</guid>        </item>
        <item>
            <title>Up-regulation of 12(S)-lipoxygenase induces a migratory phenotype in colorectal cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5602437&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22237009%26dopt%3DAbstract</link>
            <description>Authors: Klampfl T, Bogner E, Bednar W, Mager L, Massoudom D, Kalny I, Heinzle C, Berger W, Stättner S, Karner J, Klimpfinger M, Fürstenberger G, Krieg P, Marian B
    Abstract
    12(S)-Lipoxygenase (LOX) and its product 12(S)-hydroxyeicosatetraenic (HETE) acid have been implicated in angiogenesis and tumour invasion in several tumour types while their role in colorectal cancer progression has not yet been studied. We have analysed 12(S)-LOX expression in colorectal tumours and found gene expression up-regulated in colorectal cancer specimens for which the pathology report described involvement of inflammation. Using cell line models exposed to 12(S)-HETE or over-expressing 12(S)-LOX malignant cell growth as well as tumour cell migration was found to be stimulated. Specifically, Caco2 a...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5602437</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>The flavonoid eupatorin inactivates the mitotic checkpoint leading to polyploidy and apoptosis.</title>
            <link>http://www.medworm.com/index.php?rid=5578541&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22227008%26dopt%3DAbstract</link>
            <description>Authors: Salmela AL, Pouwels J, Kukkonen-Macchi A, Waris S, Toivonen P, Jaakkola K, Mäki-Jouppila J, Kallio L, Kallio MJ
    Abstract
    The spindle assembly checkpoint (SAC) is a conserved mechanism that ensures the fidelity of chromosome distribution in mitosis by preventing anaphase onset until the correct bipolar microtubule-kinetochore attachments are formed. Errors in SAC function may contribute to tumorigenesis by inducing numerical chromosome anomalies (aneuploidy). On the other hand, total disruption of SAC can lead to massive genomic imbalance followed by cell death, a phenomena that has therapeutic potency. We performed a cell-based high-throughput screen with a compound library of 2000 bioactives for novel SAC inhibitors and discovered a plant-derived phenolic compound eupato...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578541</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Characterization of mechanical behavior of an epithelial monolayer in response to epidermal growth factor stimulation.</title>
            <link>http://www.medworm.com/index.php?rid=5578540&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22227009%26dopt%3DAbstract</link>
            <description>This study also demonstrates that a combination of AFM and QCM-D is able to provide a more complete and refined mechanical profile of the cells during cell signaling.
    PMID: 22227009 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578540</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578540</guid>        </item>
        <item>
            <title>Hyaluronic acid influence on platelet-induced airway smooth muscle cell proliferation.</title>
            <link>http://www.medworm.com/index.php?rid=5578539&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22227408%26dopt%3DAbstract</link>
            <description>In conclusion, our findings demonstrate that ECM has the ability to influence platelet-induced ASMC proliferation. Specifically, we propose that HA produced by ASMC is recognised by platelet CD44. The platelet/HA interaction is followed by FAK activation and increased proliferation of co-cultured ASMC. We also suggest that the mitogenic effect of platelets represents a potential important and novel mechanism that may contribute to airway remodelling.
    PMID: 22227408 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578539</comments>
            <pubDate>Tue, 27 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578539</guid>        </item>
        <item>
            <title>Abrogation of Gli3 expression suppresses the growth of colon cancer cells via activation of p53.</title>
            <link>http://www.medworm.com/index.php?rid=5578538&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22227409%26dopt%3DAbstract</link>
            <description>Authors: Kang HN, Oh SC, Kim JS, Yoo YA
    Abstract
    p53, the major human tumor suppressor, appears to be related to sonic hedgehog (Shh)-Gli-mediated tumorigenesis. However, the role of p53 in tumor progression by the Shh-Gli signaling pathway is poorly understood. Herein we investigated the critical regulation of Gli3-p53 in tumorigenesis of colon cancer cells and the molecular mechanisms underlying these effects. RT-PCR analysis indicated that the mRNA level of Shh and Gli3 in colon tumor tissues was significantly higher than corresponding normal tissues (P&amp;lt;0.001). The inhibition of Gli3 by treatment with Gli3 siRNA resulted in a clear decrease in cell proliferation and enhanced the level of expression of p53 proteins compared to treatment with control siRNA. The half-life of p53...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578538</comments>
            <pubDate>Tue, 27 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578538</guid>        </item>
        <item>
            <title>Comment to: &quot;Spontaneous transformation of adult mesenchymal stem cells from cynomolgus macaques in vitro&quot; by Z. Ren et al. Exp. Cell Res. 317 (2011) 2950-2957, In Press Spontaneous transformation of mesenchymal stem cells in culture: Facts or fiction?</title>
            <link>http://www.medworm.com/index.php?rid=5578537&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22227410%26dopt%3DAbstract</link>
            <description>Comment to: &quot;Spontaneous transformation of adult mesenchymal stem cells from cynomolgus macaques in vitro&quot; by Z. Ren et al. Exp. Cell Res. 317 (2011) 2950-2957, In Press Spontaneous transformation of mesenchymal stem cells in culture: Facts or fiction?
    Exp Cell Res. 2011 Dec 27;
    Authors: Torsvik A, Røsland GV, Bjerkvig R
    Abstract
    There is at present a controversy in the literature whether MSCs are susceptible to spontaneous in vitro transformation or not. Several groups have reported spontaneous transformation of MSCs from various species. However, some of these reports were not true transformations and later proven to be due to cross-contaminating cancer cells. To date there is no solid evidence that MSCs can undergo spontaneous transformation in culture. Only two groups ...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578537</comments>
            <pubDate>Tue, 27 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578537</guid>        </item>
        <item>
            <title>Flagellin/TLR5 responses induce mucus hypersecretion by activating EGFR via an epithelial cell signaling cascades.</title>
            <link>http://www.medworm.com/index.php?rid=5578536&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22227411%26dopt%3DAbstract</link>
            <description>Authors: Yu H, Zhou X, Wen S, Xiao Q
    Abstract
    Mucus hypersecretion is an important manifestation in patients with chronic inflammatory airway diseases. Excessive production of mucin leads to airway mucus obstruction and contributes to morbidity and mortality in these diseases. The molecular mechanisms underlying mucin overproduction, however, still remain largely unknown. Here, we report that the bacterium Pseudomonas aeruginosa (P. aeruginosa), an important human respiratory pathogen, induced MUC5AC mucin expression via an epithelial cell signaling cascade in human airway epithelial cells. The flagellin purified from P. aeruginosa up-regulated MUC5AC expression by activating its receptor Toll-like receptor 5 (TLR5) in 16HBE cells. This effect was inhibited by NADPH oxidase inhibit...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578536</comments>
            <pubDate>Tue, 27 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578536</guid>        </item>
        <item>
            <title>MNK1 expression increases during cellular senescence and modulates the subcellular localization of hnRNP A1.</title>
            <link>http://www.medworm.com/index.php?rid=5578535&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22227431%26dopt%3DAbstract</link>
            <description>In this study, we have explored the possible involvement of MNK1, one of the downstream effector of p38 MAPK, in the regulation of hnRNP A1. We have demonstrated that pharmacological inhibition of MNK1 by CGP 57380 decreased the phosphorylation levels of hnRNP A1 in young and senescent fibroblast cells and blocked the cytoplasmic accumulation of hnRNP A1 in senescent cells. In addition, MNK1 formed a complex with hnRNP A1 in vivo. The expression levels of MNK1, phospho-MNK1, and phospho-eIF4E proteins were found to be elevated in senescent cells. These data suggest that MNK1 regulates the phosphorylation and the subcellular distribution of hnRNP A1 and that MNK1 may play a role in the induction of senescence.
    PMID: 22227431 [PubMed - as supplied by publisher] (Source: Experimental Cell...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578535</comments>
            <pubDate>Tue, 27 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578535</guid>        </item>
        <item>
            <title>Krüppel-like factor 4 regulates membranous and endochondral ossification.</title>
            <link>http://www.medworm.com/index.php?rid=5578543&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22206865%26dopt%3DAbstract</link>
            <description>Authors: Michikami I, Fukushi T, Tanaka M, Egusa H, Maeda Y, Ooshima T, Wakisaka S, Abe M
    Abstract
    Krüppel-like factor 4 (KLF4/GKLF/EZF) is a zinc finger type of transcription factor highly expressed in the skin, intestine, testis, lung and bone. The role played by Klf4 has been studied extensively in normal epithelial development and maintenance; however, its role in bone cells is unknown. Previous reports showed that Klf4 is expressed in the developing flat bones but its expression diminishes postnatally. We now show that in the developing long bones, Klf4 is expressed in the perichondrium, trabecular osteoblasts and prehypertrophic chondrocytes. In contrast, osteoblasts lining at the surface of the bone collar showed extremely low levels of Klf4 expression. To investigate the p...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578543</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578543</guid>        </item>
        <item>
            <title>Spontaneous transformation of cynomolgus mesenchymal stem cells in vitro: Further confirmation by short tandem repeat analysis.</title>
            <link>http://www.medworm.com/index.php?rid=5578542&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22206866%26dopt%3DAbstract</link>
            <description>In this study, we continued with our previous finding of spontaneous transformation of cynomolgus MSCs and provided further evidence using short tandem repeat analysis that the transformed mesenchymal stem cells were indeed derived from cynomolgus MSCs.
    PMID: 22206866 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578542</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5578542</guid>        </item>
        <item>
            <title>Human amniotic epithelial cell feeder layers maintain human iPS cell pluripotency via inhibited endogenous microRNA-145 and increased Sox2 expression.</title>
            <link>http://www.medworm.com/index.php?rid=5550433&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22200372%26dopt%3DAbstract</link>
            <description>Authors: Liu T, Cheng W, Huang Y, Huang Q, Jiang L, Guo L
    Abstract
    Currently, human induced pluripotent stem (iPS) cells were generated from patient or disease-specific sources and share the same key properties as embryonic stem cells. This makes them attractive for personalized medicine, drug screens or cellular therapy. Long-term cultivation and maintenance of normal iPS cells in an undifferentiated self-renewing state are a major challenge. Our previous studies have shown that human amniotic epithelial cells (HuAECs) could provide a good source of feeder cells for mouse and human embryonic stem cells, or spermatogonial stem cells, but the mechanism for this is unknown. Here, we examined the effect of endogenous microRNA-145 regulation on Sox2 expression in human iPS cells by HuA...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550433</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550433</guid>        </item>
        <item>
            <title>Differential effects on cell motility, embryonic stem cell self-renewal and senescence by diverse Src kinase family inhibitors.</title>
            <link>http://www.medworm.com/index.php?rid=5550437&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22197704%26dopt%3DAbstract</link>
            <description>Authors: Tamm C, Galitó SP, Annerén C
    Abstract
    The Src family of non-receptor tyrosine kinases (SFKs) has been shown to play an intricate role in embryonic stem (ES) cell maintenance. In the present study we have focused on the underlying molecular mechanisms responsible for the vastly different effects induced by various commonly used SFK inhibitors. We show that several diverse cell types, including fibroblasts completely lacking SFKs, cannot undergo mitosis in response to SU6656 and that this is caused by an unselective inhibition of Aurora kinases. In contrast, PP2 and PD173952 block motility immediately upon exposure and forces cells to grow in dense colonies. The subsequent halt in proliferation of fibroblast and epithelial cells in the center of the colonies approximately ...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550437</comments>
            <pubDate>Sat, 17 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550437</guid>        </item>
        <item>
            <title>Reconstitution of the cellular response to DNA damage in vitro using damage-activated extracts from mammalian cells.</title>
            <link>http://www.medworm.com/index.php?rid=5550436&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22197705%26dopt%3DAbstract</link>
            <description>Authors: Roper K, Coverley D
    Abstract
    In proliferating mammalian cells, DNA damage is detected by sensors that elicit a cellular response which arrests the cell cycle and repairs the damage. As part of the DNA damage response, DNA replication is inhibited and, within seconds, histone H2AX is phosphorylated. Here we describe a cell-free system that reconstitutes the cellular response to DNA double strand breaks using damage-activated cell extracts and naïve nuclei. Using this system the effect of damage signalling on nuclei that do not contain DNA lesions can be studied, thereby uncoupling signalling and repair. Soluble extracts from G1/S phase cells that were treated with etoposide before isolation, or pre-incubated with nuclei from etoposide-treated cells during an in vitro activ...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550436</comments>
            <pubDate>Fri, 16 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550436</guid>        </item>
        <item>
            <title>The axonal repellent Slit2 inhibits pericyte migration: Potential implications in angiogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5550435&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22198087%26dopt%3DAbstract</link>
            <description>Authors: Guijarro-Muñoz I, Cuesta AM, Alvarez-Cienfuegos A, Geng JG, Alvarez-Vallina L, Sanz L
    Abstract
    The Slit family of secreted proteins acts through the Roundabout (Robo) receptors to repel axonal migration during central nervous system development. Emerging evidence shows that Slit/Robo interactions also play a role in angiogenesis. The effect of Robo signaling on endothelial cells has been shown to be context-dependent. However, the role of Slit/Robo in pericytes has been largely unexplored. The aim of this study was to determine the effect of Slit2 on primary human pericytes and to address the underlying mechanisms, including the receptors potentially implicated. We demonstrate that both Robo1 and Robo4 are expressed by human pericytes. In the presence of their ligand Slit...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550435</comments>
            <pubDate>Wed, 14 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550435</guid>        </item>
        <item>
            <title>The significance of the host inflammatory response on the therapeutic efficacy of cell therapies utilising human adult stem cells.</title>
            <link>http://www.medworm.com/index.php?rid=5550434&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22198088%26dopt%3DAbstract</link>
            <description>Authors: Navarro M, Pu F, Hunt JA
    Abstract
    Controlling the fate of implanted hMSCs is one of the major drawbacks to be overcome to realize tissue engineering strategies. In particular, the effect of the inflammatory environment on hMSCs behaviour is poorly understood. Studying and mimicking the inflammatory process in vitro is a very complex and challenging task that involves multiple variables. This research addressed the questions using in vitro co-cultures of primary derived hMSCs together with human peripheral blood mononucleated cells (PBMCs); the latter are key agents in the inflammatory process. This work explored the in vitro phenotypic changes of hMSCs in co-culture direct contact with monocytes and lymphocytes isolated from blood using both basal and osteogenic medium. Ou...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550434</comments>
            <pubDate>Wed, 14 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550434</guid>        </item>
        <item>
            <title>Mutations and epimutations in the origin of cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5535281&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22182599%26dopt%3DAbstract</link>
            <description>Authors: Peltomäki P
    Abstract
    Cancer is traditionally viewed as a disease of abnormal cell proliferation controlled by a series of mutations. Mutations typically affect oncogenes or tumor suppressor genes thereby conferring growth advantage. Genomic instability facilitates mutation accumulation. Recent findings demonstrate that activation of oncogenes and inactivation of tumor suppressor genes, as well as genomic instability, can be achieved by epigenetic mechanisms as well. Unlike genetic mutations, epimutations do not change the base sequence of DNA and are potentially reversible. Similar to genetic mutations, epimutations are associated with specific patterns of gene expression that are heritable through cell divisions. Knudson's hypothesis postulates that inactivation of tumor...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535281</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5535281</guid>        </item>
        <item>
            <title>Long-term in-vivo tumorigenic assessment of human culture-expanded adipose stromal/stem cells.</title>
            <link>http://www.medworm.com/index.php?rid=5535280&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22185824%26dopt%3DAbstract</link>
            <description>In this study, a high dose of culture expanded ASCs was formulated and implanted as multicellular aggregates into immunocompromised mice, which were maintained for over one year. Animals were monitored for toxicity, and surviving cells quantified at study endpoint. No difference in growth/weight or lifespan was found between cell-treated and vehicle treated animals, and no malignancies were detected in treated animals. Moreover, real-time PCR for a human specific sequence, ERV-3, detected no persistent ASCs. With the advent of clinical application, clarification of currently enigmatic stem cell properties has become imperative. Our study represents the longest duration determination of stem cell activity in vivo, and contributes strong evidence in support of the safety of adipose derived s...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535280</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5535280</guid>        </item>
        <item>
            <title>Lactate is a mediator of metabolic cooperation between stromal carcinoma associated fibroblasts and glycolytic tumor cells in the tumor microenvironment.</title>
            <link>http://www.medworm.com/index.php?rid=5535282&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22178238%26dopt%3DAbstract</link>
            <description>Authors: Rattigan YI, Patel BB, Ackerstaff E, Sukenick G, Koutcher JA, Glod JW, Banerjee D
    Abstract
    Human mesenchymal stem cells (hMSCs) are bone marrow-derived stromal cells, which play a role in tumor progression. We have shown earlier that breast cancer cells secrete higher levels of interleukin-6 (IL-6) under hypoxia, leading to the recruitment of hMSCs towards hypoxic tumor cells. We found that (i) MDA-MB-231 cells secrete significantly higher levels of lactate (3-fold more) under hypoxia (1% O(2)) than under 20% O(2) and (ii) lactate recruits hMSCs towards tumor cells by activating signaling pathways to enhance migration. The mRNA and protein expression of functional MCT1 in hMSCs is increased in response to lactate exposure. Thus, we hypothesized that hMSCs and stromal carci...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535282</comments>
            <pubDate>Thu, 08 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5535282</guid>        </item>
        <item>
            <title>Generation of reactive oxygen species (ROS) is a key factor for stimulation of macrophage proliferation by ceramide 1-phosphate.</title>
            <link>http://www.medworm.com/index.php?rid=5535284&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22155727%26dopt%3DAbstract</link>
            <description>Authors: Arana L, Gangoiti P, Ouro A, Rivera IG, Ordoñez M, Trueba M, Lankalapalli RS, Bittman R, Gomez-Muñoz A
    Abstract
    We previously demonstrated that ceramide 1-phosphate (C1P) is mitogenic for fibroblasts and macrophages. However, the mechanisms involved in this action were only partially described. Here, we demonstrate that C1P stimulates reactive oxygen species (ROS) formation in primary bone marrow-derived macrophages, and that ROS are required for the mitogenic effect of C1P. ROS production was dependent upon prior activation of NADPH oxidase by C1P, which was determined by measuring phosphorylation of the p40phox subunit and translocation of p47phox from the cytosol to the plasma membrane. In addition, C1P activated cytosolic calcium-dependent phospholipase A(2) and prot...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535284</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5535284</guid>        </item>
        <item>
            <title>Valproic acid affects the engraftment of TPO-expanded cord blood cells in NOD/SCID mice.</title>
            <link>http://www.medworm.com/index.php?rid=5535283&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22166516%26dopt%3DAbstract</link>
            <description>Authors: Vulcano F, Milazzo L, Ciccarelli C, Barca A, Agostini F, Altieri I, Macioce G, Di Virgilio A, Screnci M, De Felice L, Giampaolo A, Hamisa JH
    Abstract
    Hematopoietic stem and progenitor cells (HSPC) can improve the long-term outcome of transplanted individuals and reduce the relapse rate. Valproic acid (VPA), an inhibitor of histone deacetylase, when combined with different cytokine cocktails, induces the expansion of CD34+ cell populations derived from cord blood (CB) and other sources. We evaluated the effect of VPA, in combination with thrombopoietin (TPO), on the viability and expansion of CB-HSPCs and on short- and long-term engraftability in the NOD/SCID mouse model. In vitro, VPA+TPO inhibited HSPC differentiation and preserved the CD34+ cell fraction; the self-renewa...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535283</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5535283</guid>        </item>
        <item>
            <title>Transcriptional profiling identifies upregulated genes following induction of epithelial-mesenchymal transition in squamous carcinoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=5535285&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22154512%26dopt%3DAbstract</link>
            <description>In this study, expression microarray analysis identified a set of 145 upregulated genes in EMT-like HNSCC cells. Some of the strongly upregulated transcripts include genes that are reportedly involved in invasion and metastasis, such as DOCK10, LOX, ROBO1 and SRGN. Importantly, the Tbx3 gene, a member of the T-box transcription factor, was strongly upregulated in SCC cells displaying an EMT-like phenotype compared to cells with an epitheloid, non-EMT behavior. Tbx3 was also found to be strongly upregulated at the protein and gene expression level in an experimental model of snail-induced EMT cells. In addition, siRNA-induced Tbx3 depletion modestly suppressed cell invasion while enhancing Tbx3-mediated resistance to anoikis. Our findings provide evidence that Tbx3 overexpression promotes S...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535285</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5535285</guid>        </item>
        <item>
            <title>Transmyocardial drilling revascularization combined with heparinized bFGF-incorporating stent activates resident cardiac stem cells via SDF-1/CXCR4 axis.</title>
            <link>http://www.medworm.com/index.php?rid=5535288&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22146760%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: The new method has shown to be capable of promoting CSCs proliferation and differentiation into cardiomyocytes through activating the SDF-1/CXCR4 axis, while inhibiting myocardial apoptosis, thereby enhancing myocardial regeneration following AMI and improving cardiac function. This may provide a new strategy for myocardial regeneration following AMI.
    PMID: 22146760 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535288</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5535288</guid>        </item>
        <item>
            <title>ER signaling regulation drives the switch between autophagy and apoptosis in NRK-52E cells exposed to cisplatin.</title>
            <link>http://www.medworm.com/index.php?rid=5535287&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22146761%26dopt%3DAbstract</link>
            <description>Authors: Rovetta F, Stacchiotti A, Consiglio A, Cadei M, Grigolato PG, Lavazza A, Rezzani R, Aleo MF
    Abstract
    Cisplatin (cisPt) use in chemotherapy is limited by the occurrence of a severe nephrotoxicity. Both autophagy and apoptosis seem to contribute in kidney response to cisPt, however their cross-talk is still controversial, since the role played by autophagy (cytoprotective or harmful) and the cellular site driving their switch, are still unclear. Here, we used a multidisciplinary approach to study the correlation between autophagy and apoptosis in renal NRK-52E cells exposed to cisPt. We show two &quot;sensitivity-thresholds&quot; to cisPt, stating whether apoptosis or autophagy would develop: 10μM dose of cisPt activated autophagy that preserved cell homeostasis; however 3-methyladen...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535287</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5535287</guid>        </item>
        <item>
            <title>Role for Class I histone deacetylases in multidrug resistance.</title>
            <link>http://www.medworm.com/index.php?rid=5535286&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22154511%26dopt%3DAbstract</link>
            <description>In this study, HDAC1 and HDAC2 acted as enhancers to intensify the chemosensitivities of anti-cancer drugs via reducing the expression levels of P-gp, MRP1 and MRP2. Furthermore, the dissociation of HDAC1 and HDAC2 led to transcriptional regulation of P-gp expression via the recruitment of p300, PCAF and NF-Y to the P-gp promoter region, which subsequently increased the level of the active gene marker, hyperacetylated histone H3. In parallel, selective inhibition of HDAC1 and HDAC2 induced the recruitment of p300, PCAF, NF-Y via acetylation of Sp1. Thus, our findings showed HDAC1 and 2 regulated P-gp expression through dynamic changes in chromatin structure and transcription factor association within the promoter region.
    PMID: 22154511 [PubMed - as supplied by publisher] (Source: Exper...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535286</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5535286</guid>        </item>
        <item>
            <title>Stem cells as the root of pancreatic ductal adenocarcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=5475512&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22119145%26dopt%3DAbstract</link>
            <description>Authors: Balic A, Dorado J, Alonso-Gómez M, Heeschen C
    Abstract
    Emerging evidence suggests that stem cells play a crucial role not only in the generation and maintenance of different tissues, but also in the development and progression of malignancies. For the many solid cancers, it has now been shown that they harbor a distinct subpopulation of cancer cells that bear stem cell features and therefore, these cells are termed cancer stem cells (CSC) or tumor-propagating cells. CSC are exclusively tumorigenic and essential drivers for tumor progression and metastasis. Moreover, it has been shown that pancreatic ductal adenocarcinoma does not only contain one homogeneous population of CSC rather than diverse subpopulations that may have evolved during tumor progression. One of these p...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475512</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475512</guid>        </item>
        <item>
            <title>A mutation of the fission yeast EB1 overcomes negative regulation by phosphorylation and stabilizes microtubules.</title>
            <link>http://www.medworm.com/index.php?rid=5475511&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22134091%26dopt%3DAbstract</link>
            <description>Authors: Iimori M, Ozaki K, Chikashige Y, Habu T, Hiraoka Y, Maki T, Hayashi I, Obuse C, Matsumoto T
    Abstract
    Mal3 is a fission yeast homolog of EB1, a plus-end tracking protein (+TIP). We have generated a mutation (89R) replacing glutamine with arginine in the calponin homology (CH) domain of Mal3. Analysis of the 89R mutant in vitro has revealed that the mutation confers a higher affinity to microtubules and enhances the intrinsic activity to promote the microtubule-assembly. The mutant Mal3 is no longer a +TIP, but binds strongly the microtubule lattice. Live cell imaging has revealed that while the wild type Mal3 proteins dissociate from the tip of the growing microtubules before the onset of shrinkage, the mutant Mal3 proteins persist on microtubules and reduces a rate of shri...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475511</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475511</guid>        </item>
        <item>
            <title>A methionine-choline-deficient diet elicits NASH in the immunodeficient mouse featuring a model for hepatic cell transplantation.</title>
            <link>http://www.medworm.com/index.php?rid=5475514&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22108588%26dopt%3DAbstract</link>
            <description>Authors: Pelz S, Stock P, Brückner S, Christ B
    Abstract
    Non-alcoholic staetohepatitis (NASH) is associated with fat deposition in the liver favoring inflammatory processes and development of fibrosis, cirrhosis and finally hepatocellular cancer. In Western lifestyle countries, NASH has reached a 20% prevalence in the obese population with escalating tendency in the future. Very often, liver transplantation is the only therapeutic option. Recently, transplantation of hepatocyte-like cells differentiated from mesenchymal stem cells was suggested a feasible alternative to whole organ transplantation to ameliorate donor organ shortage. Hence, in the present work an animal model of NASH was established in immunodeficient mice to investigate the feasibility of human stem cell-derived he...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475514</comments>
            <pubDate>Sun, 13 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475514</guid>        </item>
        <item>
            <title>Toll-like receptors 2 and 4 mediate the capacity of mesenchymal stromal cells to support the proliferation and differentiation of CD34(+) cells.</title>
            <link>http://www.medworm.com/index.php?rid=5475517&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22100911%26dopt%3DAbstract</link>
            <description>In this study, we investigated the possible role(s) of TLRs in mediating the hematopoiesis-supporting role of human BM-MSCs. Human BM-MSCs were analyzed for mRNA expression of TLR1-10 by reverse transcription-polymerase chain reaction. TLR1-6, but not TLR7-10 were expressed by BM-MSCs. The protein expression of TLR2 and TLR4 was also confirmed by flow cytometry. We further explored the role of TLR2 and TLR4 in mediating the capacity of BM-MSCs to support the proliferation and differentiation of CD34(+) hematopoietic stem/progenitor cells obtained from cord blood. BM-MSCs increased proliferation of CD34(+) cells and promoted the differentiation towards the myeloid lineage 7 or 14days after co-culture, as well as colony formation by those cells and the production of interleukin 1 (IL-1), IL-...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475517</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475517</guid>        </item>
        <item>
            <title>The human HECA interacts with cyclins and CDKs to antagonize Wnt-mediated proliferation and chemoresistance of head and neck cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5475516&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22100912%26dopt%3DAbstract</link>
            <description>Authors: Dowejko A, Bauer R, Bauer K, Müller-Richter UD, Reichert TE
    Abstract
    There is a growing evidence that the human homologue of the Drosophila headcase (HECA) plays an important role in human carcinogenesis. So far specific protein interaction partners and affected signaling pathways of HECA are still elusive. In a recent study we showed that HECA overexpression in oral squamous-cell carcinoma (OSCC) keratinocytes has tumor suppressive effects resulting in a recuperation of cell cycle control concerning the entry and progression of S-phase, G2- and M-phase. Currently, quantitative RT-PCR and immunohistochemical analysis of primary tumor tissue from OSCC patients demonstrate that HECA expression is markedly decreased compared to normal control patients with abundant HECA expr...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475516</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475516</guid>        </item>
        <item>
            <title>Stable expression of lipocalin-type prostaglandin D synthase in cultured preadipocytes impairs adipogenesis program independently of endogenous prostanoids.</title>
            <link>http://www.medworm.com/index.php?rid=5475515&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22100987%26dopt%3DAbstract</link>
            <description>Authors: Hossain MS, Chowdhury AA, Rahman MS, Nishimura K, Jisaka M, Nagaya T, Shono F, Yokota K
    Abstract
    Lipocalin-type prostaglandin D synthase (L-PGDS) expressed preferentially in adipocytes is responsible for the synthesis of PGD(2) and its non-enzymatic dehydration products, PGJ(2) series, serving as pro-adipogenic factors. However, the role of L-PGDS in the regulation of adipogenesis is complex because of the occurrence of several derivatives from PGD(2) and their distinct receptor subtypes as well as other functions such as a transporter of lipophilic molecules. To manipulate the expression levels of L-PGDS in cultured adipocytes, cultured preadipogenic 3T3-L1 cells were transfected stably with a mammalian expression vector having cDNA encoding murine L-PGDS oriented in the ...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475515</comments>
            <pubDate>Wed, 09 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475515</guid>        </item>
        <item>
            <title>Microphthalmia-associated transcription factor acts through PEDF to regulate RPE cell migration.</title>
            <link>http://www.medworm.com/index.php?rid=5475513&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22115973%26dopt%3DAbstract</link>
            <description>Authors: Ma X, Pan L, Jin X, Dai X, Li H, Wen B, Chen Y, Ma A, Qu J, Hou L
    Abstract
    Cells of the retinal pigment epithelium (RPE) play major roles in metabolic functions, maintenance of photoreceptor function, and photoreceptor survival in the retina. They normally form a stable monolayer, but migrate during disease states. Although growth factors produced by the RPE cells primarily control these cellular events, how these factors are regulated in RPE cells remain largely unknown. Here we show that the basic-helix-loop-helix-leucine zipper microphthalmia-associated transcription factor (MITF), which plays central roles in the development and function of a variety of cell types including RPE cells, upregulates the expression of a multifunctional factor PEDF in RPE cells. Consequentl...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475513</comments>
            <pubDate>Wed, 09 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475513</guid>        </item>
        <item>
            <title>A novel proapoptotic gene PANO encodes a post-translational modulator of the tumor suppressor p14ARF.</title>
            <link>http://www.medworm.com/index.php?rid=5475519&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22094112%26dopt%3DAbstract</link>
            <description>Authors: Watari A, Li Y, Higashiyama S, Yutsudo M
    Abstract
    The protein p14ARF is a known tumor suppressor protein controlling cell proliferation and survival, which mainly localizes in nucleoli. However, the regulatory mechanisms that govern its activity or expression remain unclear. Here, we report that a novel proapoptotic nucleolar protein, PANO, modulates the expression and activity of p14ARF in HeLa cells. Overexpression of PANO enhances the stability of p14ARF protein by protecting it from degradation, resulting in an increase in p14ARF expression levels. Overexpression of PANO also induces apoptosis under low serum conditions. This effect is dependent on the nucleolar localization of PANO and inhibited by knocking-down p14ARF. Alternatively, PANO siRNA treated cells exhibit ...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475519</comments>
            <pubDate>Mon, 07 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475519</guid>        </item>
        <item>
            <title>Epigenetic and transcriptional control of the 15-lipoxygenase-1 gene in a Hodgkin lymphoma cell line.</title>
            <link>http://www.medworm.com/index.php?rid=5475518&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22094113%26dopt%3DAbstract</link>
            <description>Authors: Liu C, Schain F, Han H, Xu D, Andersson-Sand H, Forsell P, Claesson HE, Björkholm M, Sjöberg J
    Abstract
    Lipoxygenases oxidatively metabolize polyunsaturated fatty acids to a rich spectrum of biologically active metabolites. The present study aimed at delineating the transcriptional and epigenetic mechanisms leading to 15-lipoxygenase-1 (15-LOX-1) expression in the Hodgkin lymphoma (HL) cell line L1236. Examination of the 15-LOX-1 5' promoter region demonstrated three putative binding sites for signal transducer and activator of transcription (STAT6) within the proximal 1200 base pairs relative to the start codon. Analysis by serial promoter deletions and STAT6 binding site mutations indicated that all three STAT6 binding sites are required for full activation of the 15-L...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5475518</comments>
            <pubDate>Mon, 07 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5475518</guid>        </item>
        <item>
            <title>CNK3 and IPCEF1 produce a single protein that is required for HGF dependent Arf6 activation and migration.</title>
            <link>http://www.medworm.com/index.php?rid=5421501&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22085542%26dopt%3DAbstract</link>
            <description>We report here that IPCEF1 is actually the C-terminal half of CNK3. CNKs are scaffolds involved in signal transduction downstream of Ras. We have found that both MDCK and CaCo-2 cells express a fused CNK3/IPCEF1 protein. Knockdown of this protein impairs HGF-induced Arf6 activation and migration in response to HGF treatment.
    PMID: 22085542 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5421501</comments>
            <pubDate>Mon, 07 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5421501</guid>        </item>
        <item>
            <title>Leucine limitation regulates myf5 and myoD expression and inhibits myoblast differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=5421503&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22079119%26dopt%3DAbstract</link>
            <description>This study demonstrates the importance of a nutrient, leucine, in the control of the myogenic differentiation program.
    PMID: 22079119 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5421503</comments>
            <pubDate>Thu, 03 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5421503</guid>        </item>
        <item>
            <title>Visualizing the effect of hypoxia on fluorescence kinetics in living HeLa cells using the fluorescent ubiquitination-based cell cycle indicator (Fucci).</title>
            <link>http://www.medworm.com/index.php?rid=5421502&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22079518%26dopt%3DAbstract</link>
            <description>Authors: Kaida A, Miura M
    Abstract
    Fluorescent proteins are widely used for the direct visualization of events such as gene expression and subcellular localization in mammalian cells. It is well established that oxygen is required for formation of functional chromophore; however, the effect of hypoxia on fluorescence emission has rarely been studied. For this purpose, under hypoxic conditions, we investigated the kinetics of red and green fluorescence in HeLa cells from two fluorescent proteins, monomeric Kusabira Orange 2 (mKO2) and monomeric Azami Green (mAG), respectively, using the fluorescent ubiquitination-based cell cycle indicator (Fucci). In this system, cells in G1 or other phases emit red or green fluorescence, respectively. We found that hypoxia abrogated both red and g...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5421502</comments>
            <pubDate>Thu, 03 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5421502</guid>        </item>
        <item>
            <title>Changes in inflammatory gene expression induced by hyperbaric oxygen treatment in human endothelial cells under chronic wound conditions.</title>
            <link>http://www.medworm.com/index.php?rid=5421504&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22063471%26dopt%3DAbstract</link>
            <description>Authors: Kendall AC, Whatmore JL, Harries LW, Winyard PG, Smerdon GR, Eggleton P
    Abstract
    Hyperbaric oxygen (HBO) therapy involves the inhalation of 100% oxygen, whilst inside a chamber at greater than atmospheric pressure. It is an effective treatment for chronic diabetic wounds, although the molecular mechanisms involved remain unclear. We hypothesised that HBO could alter inflammatory gene expression in human endothelial cells via a reactive oxygen/nitrogen species-mediated pathway. Endothelial cells were exposed to a chronic wound model comprising hypoxia (2% O(2) at 1 atmosphere absolute (ATA); PO(2) ~2kPa) in the presence of lipopolysaccharide and TNF-α for 24h, then treated with HBO for 90min (97.5% O(2) at 2.4 ATA; PO(2) ~237kPa). 5h post-HBO, 19 genes involved in adhesion...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5421504</comments>
            <pubDate>Fri, 28 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5421504</guid>        </item>
        <item>
            <title>Cell aging-induced methionine oxidation causes an autocrine to paracrine shift of the pheromone activity in the protozoan ciliate, Euplotes raikovi.</title>
            <link>http://www.medworm.com/index.php?rid=5380054&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22036647%26dopt%3DAbstract</link>
            <description>Authors: Alimenti C, Vallesi A, Luporini P, Buonanno F, Ortenzi C
    Abstract
    Ciliates of the genus Euplotes rely on the autocrine (self) and paracrine (non-self) activities of their water-borne protein pheromones to control the two fundamental phenomena of their life cycle, i.e. vegetative (mitotic) growth and sex manifested as cell union in mating pairs. We observed that cell aging determines the synthesis of increasing concentrations of pheromones that are oxidized at the level of methionine residues which are more exposed on the molecular surface. The oxidized form of the E. raikovi pheromone Er-1 was purified and its interactions with its source cells were shown no longer to be of autocrine type directed to promote cell growth, but changed to interactions of the paracrine type di...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5380054</comments>
            <pubDate>Fri, 21 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5380054</guid>        </item>
        <item>
            <title>Chemokines in tumor development and progression.</title>
            <link>http://www.medworm.com/index.php?rid=5380052&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22036649%26dopt%3DAbstract</link>
            <description>Authors: Mukaida N, Baba T
    Abstract
    Chemokines were originally identified as mediators of the inflammatory process and regulators of leukocyte trafficking. Subsequent studies revealed their essential roles in leukocyte physiology and pathology. Moreover, chemokines have profound effects on other types of cells associated with the inflammatory response, such as endothelial cells and fibroblasts. Thus, chemokines are crucial for cancer-related inflammation, which can promote tumor development and progression. Increasing evidence points to the vital effects of several chemokines on the proliferative and invasive properties of tumor cells. The wide range of activities of chemokines in tumorigenesis highlights their roles in tumor development and progression.
    PMID: 22036649 [PubMed ...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5380052</comments>
            <pubDate>Fri, 21 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5380052</guid>        </item>
        <item>
            <title>Increased glyoxalase I levels inhibit accumulation of oxidative stress and an advanced glycation end product in mouse mesangial cells cultured in high glucose.</title>
            <link>http://www.medworm.com/index.php?rid=5380051&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22036650%26dopt%3DAbstract</link>
            <description>Authors: Kim KM, Kim YS, Jung DH, Lee J, Kim JS
    Abstract
    Chronic high glucose levels lead to the formation of advanced glycation end-products (AGEs) as well as AGE precursors, such as methylglyoxal (MG) and glyoxal, via non-enzymatic glycation reactions in patients with diabetic mellitus. Glyoxalase 1 (GLO-1) detoxifies reactive dicarbonyls that form AGEs. To investigate the interaction between AGEs and GLO-1 in mesangial cells (MCs) under diabetic conditions, AGE levels and markers of oxidative stress were measured in GLO-1-overexpressing MCs (GLO-1-MCs) cultured in high glucose. Furthermore, we also examined levels of high glucose-induced apoptosis in GLO-1-MCs. In glomerular MCs, high glucose levels increased the formation of both MG and argpyrimidine (an MG-derived adduct) as w...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5380051</comments>
            <pubDate>Fri, 21 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5380051</guid>        </item>
        <item>
            <title>Coordinated regulation of caveolin-1 and Rab11a in apical recycling compartments of polarized epithelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=5380053&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22036648%26dopt%3DAbstract</link>
            <description>Authors: Lapierre LA, Ducharme NA, Drake KR, Goldenring JR, Kenworthy AK
    Abstract
    Recent studies have identified caveolin-1, a protein best known for its functions in caveolae, in apical endocytic recycling compartments in polarized epithelial cells. However, very little is known about the regulation of caveolin-1 in the endocytic recycling pathway. To address this question, in the current study we compared the relationship between compartments enriched in sub-apical caveolin-1 and Rab11a, a well-defined marker of apical recycling endosomes, using polarized MDCK cells as a model. We show that caveolin-1-containing vesicles define a compartment that partially overlaps with Rab11a, and that the distribution of subapical caveolin-1 and Rab11a shows a similar dependence on microtubule ...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5380053</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5380053</guid>        </item>
        <item>
            <title>Sensitization of human colon cancer cells to sodium butyrate-induced apoptosis by modulation of sphingosine kinase 2 and protein kinase D.</title>
            <link>http://www.medworm.com/index.php?rid=5380056&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22024383%26dopt%3DAbstract</link>
            <description>In this study, we investigated the role of SphK2 in NaBT-induced apoptosis of HCT116 colon cancer cells. The results indicated that following NaBT treatment SphK2 was translocated from the nucleus to the cytoplasm, leading to its accumulation in the cytoplasm; in the meantime, only mild apoptosis occurred. However, downregulation of SphK2 resulted in sensitized apoptosis, and overexpression of SphK2 led to even lighter apoptosis; these strongly indicate an inhibitory role of SphK2 in cell apoptosis induced by NaBT. After knocking down protein kinase D (PKD), another protein reported to be critical in cell proliferation/apoptosis process, by using siRNA, blockage of cytoplasmic accumulation of SphK2 and sensitized apoptosis following NaBT treatment were observed. The present study suggests ...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5380056</comments>
            <pubDate>Sat, 15 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5380056</guid>        </item>
        <item>
            <title>Interstitial fluid flow and cyclic strain differentially regulate cardiac fibroblast activation via AT1R and TGF-β1.</title>
            <link>http://www.medworm.com/index.php?rid=5380061&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22020089%26dopt%3DAbstract</link>
            <description>Authors: Galie PA, Russell MW, Westfall MV, Stegemann JP
    Abstract
    Cardiac fibroblasts are exposed to both cyclic strain and interstitial fluid flow in the myocardium. The balance of these stimuli is affected by fibrotic scarring, during which the fibroblasts transition to a myofibroblast phenotype. The present study investigates the mechanisms by which cardiac fibroblasts seeded in three-dimensional (3D) collagen gels differentiate between strain and fluid flow. Neonatal cardiac fibroblast-seeded 3D collagen gels were exposed to interstitial flow and/or cyclic strain and message levels of collagens type I and III, transforming growth factor β1 (TGF-β1), and α-smooth muscle actin (α-SMA) were assessed. Flow was found to significantly increase and strain to decrease expression of...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5380061</comments>
            <pubDate>Fri, 14 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5380061</guid>        </item>
        <item>
            <title>Synaptotagmin 1 causes phosphatidyl inositol lipid-dependent actin remodeling in cultured non-neuronal and neuronal cells.</title>
            <link>http://www.medworm.com/index.php?rid=5380055&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22036579%26dopt%3DAbstract</link>
            <description>Authors: Johnsson AK, Karlsson R
    Abstract
    Here we demonstrate that a dramatic actin polymerizing activity caused by ectopic expression of the synaptic vesicle protein synaptotagmin 1, that results in extensive filopodia formation is due to the presence of a lysine rich sequence motif immediately at the cytoplasmic side of the transmembrane domain of the protein. This polybasic sequence interacts with anionic phospholipids in vitro, and, consequently, the actin remodeling caused by this sequence is interfered with by expression of a phosphatidyl inositol (4,5)-bisphosphate (PIP2)-targeted phosphatase, suggesting that it intervenes with the function of PIP2-binding actin control proteins. The activity drastically alters the behavior of a range of cultured cells including the neurobla...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5380055</comments>
            <pubDate>Fri, 14 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5380055</guid>        </item>
        <item>
            <title>Novel approach to abuse the hyperactive K-Ras pathway for adenoviral gene therapy of colorectal cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5380060&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22020090%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: Selective targeting of CRC cells with the activated Ras pathway may be a novel and effective therapy in CRC. The high potency of this adenoviral vector may help to overcome an undetectable micro metastasis that is the major hurdle in challenging with CRC.
    PMID: 22020090 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5380060</comments>
            <pubDate>Wed, 12 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5380060</guid>        </item>
        <item>
            <title>GREG cells, a dysferlin-deficient myogenic mouse cell line.</title>
            <link>http://www.medworm.com/index.php?rid=5380059&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22020321%26dopt%3DAbstract</link>
            <description>Authors: Humphrey GW, Mekhedov E, Blank PS, de Morree A, Pekkurnaz G, Nagaraju K, Zimmerberg J
    Abstract
    The dysferlinopathies (e.g. LGMD2b, Myoshi myopathy) are progressive, adult-onset muscle wasting syndromes caused by mutations in the gene coding for dysferlin. Dysferlin is a large (~200kDa) membrane-anchored protein, required for maintenance of plasmalemmal integrity in muscle fibers. To facilitate analysis of dysferlin function in muscle cells, we have established a dysferlin-deficient myogenic cell line (GREG cells) from the A/J mouse, a genetic model for dysferlinopathy. GREG cells have no detectable dysferlin expression, but proliferate normally in growth medium and fuse into functional myotubes in differentiation medium. GREG myotubes exhibit deficiencies in plasma membran...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5380059</comments>
            <pubDate>Wed, 12 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5380059</guid>        </item>
        <item>
            <title>Fibrin glue is a candidate scaffold for long-term therapeutic protein expression in spontaneously differentiated adipocytes in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=5380058&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22020322%26dopt%3DAbstract</link>
            <description>Authors: Aoyagi Y, Kuroda M, Asada S, Tanaka S, Konno S, Tanio M, Aso M, Okamoto Y, Nakayama T, Saito Y, Bujo H
    Abstract
    Adipose tissue is expected to provide a source of cells for protein replacement therapies via auto-transplantation. However, the conditioning of the environment surrounding the transplanted adipocytes for their long-term survival and protein secretion properties has not been established. We have recently developed a preparation procedure for preadipocytes, ceiling culture-derived proliferative adipocytes (ccdPAs), as a therapeutic gene vehicle suitable for stable gene product secretion. We herein report the results of our evaluation of using fibrin glue as a scaffold for the transplanted ccdPAs for the expression of a transduced gene in a three-dimensional cultur...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5380058</comments>
            <pubDate>Wed, 12 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5380058</guid>        </item>
        <item>
            <title>Involvement of JNK and NF-κB pathways in lipopolysaccharide (LPS)-induced BAG3 expression in human monocytic cells.</title>
            <link>http://www.medworm.com/index.php?rid=5380057&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22020323%26dopt%3DAbstract</link>
            <description>Authors: Wang HQ, Meng X, Liu BQ, Li C, Gao YY, Niu XF, Li N, Guan Y, Du ZX
    Abstract
    Lipopolysaccharide (LPS) is an outer-membrane glycolipid component of Gram-negative bacteria known for its fervent ability to activate monocytic cells and for its potent proinflammatory capabilities. Bcl-2-associated athanogene 3 (BAG3) is a survival protein that has been shown to be stimulated during cell response to stressful conditions, such as exposure to high temperature, heavy metals, proteasome inhibition, and human immunodeficiency virus 1 (HIV-1) infection. In addition, BAG3 regulates replication of Varicella-Zoster Virus (VZV) and Herpes Simplex Virus (HSV) replication, suggesting that BAG3 could participate in the host response to infection. In the current study, we found that LPS increa...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5380057</comments>
            <pubDate>Wed, 12 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5380057</guid>        </item>
        <item>
            <title>Hirudin and heparin enable efficient megakaryocyte differentiation of mouse bone marrow progenitors.</title>
            <link>http://www.medworm.com/index.php?rid=5345912&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22008103%26dopt%3DAbstract</link>
            <description>Authors: Strassel C, Eckly A, Léon C, Moog S, Cazenave JP, Gachet C, Lanza F
    Abstract
    Hematopoietic progenitors from murine fetal liver efficiently differentiate in culture into proplatelet-producing megakaryocytes and have proved valuable to study platelet biogenesis. In contrast, megakaryocyte maturation is far less efficient in cultured bone marrow progenitors, which hampers studies in adult animals. It is shown here that addition of hirudin to media containing thrombopoietin and serum yielded a proportion of proplatelet-forming megakaryocytes similar to that in fetal liver cultures (approximately 50%) with well developed extensions and increased the release of platelet particles in the media. The effect of hirudin was maximal at 100U/ml, and was more pronounced when it was add...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5345912</comments>
            <pubDate>Sat, 08 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5345912</guid>        </item>
        <item>
            <title>FoxA1 and glucocorticoid receptor crosstalk via histone H4K16 acetylation at a hormone regulated enhancer.</title>
            <link>http://www.medworm.com/index.php?rid=5345917&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22001115%26dopt%3DAbstract</link>
            <description>Authors: Belikov S, Holmqvist PH, Astrand C, Wrange O
    Abstract
    The forkhead transcription factor FoxA1 participates in many gene regulatory events with steroid hormone receptors, one example being the integrated mouse mammary tumor virus (MMTV) promoter. Its enhancer harbors several FoxA1 binding sites. FoxA1 promotes glucocorticoid receptor (GR)-DNA binding and transcription. Here we analyze the regulatory capacity of GR, FoxA1 and hormone in quantitative terms when reconstituted with the MMTV enhancer in Xenopus oocytes. By titrating each component we demonstrate that FoxA1 is required for hormone induction at low GR concentration and that FoxA1 is a potent enhancer of GR-induced transcription. Conversely, specific DNA binding of FoxA1 at low intranuclear concentration is highly ...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5345917</comments>
            <pubDate>Thu, 06 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5345917</guid>        </item>
        <item>
            <title>The all-trans retinoic acid (atRA)-regulated gene Calmin (Clmn) regulates cell cycle exit and neurite outgrowth in murine neuroblastoma (Neuro2a) cells.</title>
            <link>http://www.medworm.com/index.php?rid=5345916&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22001116%26dopt%3DAbstract</link>
            <description>This study shows that the atRA-responsive gene Clmn promotes exit from the cell cycle, a requisite event for neuronal differentiation.
    PMID: 22001116 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5345916</comments>
            <pubDate>Thu, 06 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5345916</guid>        </item>
        <item>
            <title>α-Syntrophin is required for the hepatocyte growth factor-induced migration of cultured myoblasts.</title>
            <link>http://www.medworm.com/index.php?rid=5345915&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22001117%26dopt%3DAbstract</link>
            <description>In this study, we investigated the function of syntrophins in cell migration, one of the early steps in myogenic differentiation and in regeneration of adult muscle. Hepatocyte growth factor (HGF) stimulates migration and lamellipodia formation in cultured C2 myoblasts. In the migrating cells, syntrophins concentrated in the rear-lateral region of the cell, opposite of the lamellipodia, instead of being diffusely present throughout the cytoplasm of non-migrating cells. When the expression of α-syntrophin, the major syntrophin isoform of skeletal muscle, was reduced by transfection with the α-syntrophin-specific siRNA, HGF stimulation of lamellipodia formation was prevented. Likewise, migration of myoblasts from α-syntrophin knockout mice could not be stimulated by HGF. However, HGF-indu...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5345915</comments>
            <pubDate>Thu, 06 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5345915</guid>        </item>
        <item>
            <title>Dual Mode of glucagon receptor internalization: Role of PKCα, GRKs and β-arrestins.</title>
            <link>http://www.medworm.com/index.php?rid=5345914&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22001118%26dopt%3DAbstract</link>
            <description>Authors: Krilov L, Nguyen A, Miyazaki T, Unson CG, Williams R, Lee NH, Ceryak S, Bouscarel B
    Abstract
    Glucagon levels are elevated in diabetes and some liver diseases. Increased glucagon secretion leads to abnormal stimulation of glucagon receptors (GRs) and consequent elevated glucose production in the liver. Blocking glucagon receptor signaling has been proposed as a potential treatment option for diabetes and other conditions associated with hyperglycemia. Elucidating mechanisms of GR desensitization and downregulation may help identify new drug targets besides GR itself. The present study explores the mechanisms of GR internalization and the role of PKCα, GPCR kinases (GRKs) and β-arrestins therein. We have reported previously that PKCα mediates GR phosphorylation and desens...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5345914</comments>
            <pubDate>Thu, 06 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5345914</guid>        </item>
        <item>
            <title>Zac1, an Sp1-like protein, regulates human p21(WAF1/Cip1) gene expression in HeLa cells.</title>
            <link>http://www.medworm.com/index.php?rid=5345913&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22001409%26dopt%3DAbstract</link>
            <description>Authors: Liu PY, Hsieh TY, Liu ST, Chang YL, Lin WS, Wang WM, Huang SM
    Abstract
    Zac1 functions as both a transcription factor and a transcriptional cofactor for p53, nuclear receptors (NRs) and NR coactivators. Zac1 might also act as a transcriptional repressor via the recruitment of histone deacetylase 1 (HDAC1). The ability of Zac1 to interact directly with GC-specific elements indicates that Zac1 possibly binds to Sp1-responsive elements. In the present study, our data show that Zac1 is able to interact directly with the Sp1-responsive element in the p21(WAF1/Cip1) gene promoter and enhance the transactivation activity of Sp1 through direct physical interaction. Our data further demonstrate that Zac1 might enhance Sp1-specific promoter activity by interacting with the Sp1-respon...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5345913</comments>
            <pubDate>Thu, 06 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5345913</guid>        </item>
        <item>
            <title>Interaction of nucleosome assembly proteins abolishes nuclear localization of DGKζ by attenuating its association with importins.</title>
            <link>http://www.medworm.com/index.php?rid=5345918&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21996351%26dopt%3DAbstract</link>
            <description>Authors: Okada M, Hozumi Y, Ichimura T, Tanaka T, Hasegawa H, Yamamoto M, Takahashi N, Iseki K, Yagisawa H, Shinkawa T, Isobe T, Goto K
    Abstract
    Diacylglycerol kinase (DGK) is involved in the regulation of lipid-mediated signal transduction through the metabolism of a second messenger diacylglycerol. Of the DGK family, DGKζ, which contains a nuclear localization signal, localizes mainly to the nucleus but translocates to the cytoplasm under pathological conditions. However, the detailed mechanism of translocation and its functional significance remain unclear. To elucidate these issues, we used a proteomic approach to search for protein targets that interact with DGKζ. Results show that nucleosome assembly protein (NAP) 1-like 1 (NAP1L1) and NAP1-like 4 (NAP1L4) are identified as...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5345918</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5345918</guid>        </item>
        <item>
            <title>Subcellular localization of SREBP1 depends on its interaction with the C-terminal region of wild-type and disease related A-type lamins.</title>
            <link>http://www.medworm.com/index.php?rid=5313248&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21993218%26dopt%3DAbstract</link>
            <description>Authors: Duband-Goulet I, Woerner S, Gasparini S, Attanda W, Kondé E, Tellier-Lebègue C, Craescu CT, Gombault A, Roussel P, Vadrot N, Vicart P, Ostlund C, Worman HJ, Zinn-Justin S, Buendia B
    Abstract
    Lamins A and C are nuclear intermediate filament proteins expressed in most differentiated somatic cells. Previous data suggested that prelamin A, the lamin A precursor, accumulates in some lipodystrophy syndromes caused by mutations in the lamin A/C gene, and binds and inactivates the sterol regulatory element binding protein 1 (SREBP1). Here we show that, in vitro, the tail regions of prelamin A, lamin A and lamin C bind a polypeptide of SREBP1. Such interactions also occur in HeLa cells, since expression of lamin tail regions impedes nucleolar accumulation of the SREBP1 polypeptid...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313248</comments>
            <pubDate>Tue, 04 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313248</guid>        </item>
        <item>
            <title>UBR1 promotes protein kinase quality control and sensitizes cells to Hsp90 inhibition.</title>
            <link>http://www.medworm.com/index.php?rid=5313249&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21983172%26dopt%3DAbstract</link>
            <description>Authors: Sultana R, Theodoraki MA, Caplan AJ
    Abstract
    UBR1 and UBR2 are N-recognin ubiquitin ligases that function in the N-end rule degradation pathway. In yeast, the UBR1 homologue also functions by N-end rule independent means to promote degradation of misfolded proteins generated by treatment of cells with geldanamycin, a small molecule inhibitor of Hsp90. Based on these studies we examined the role of mammalian UBR1 and UBR2 in the degradation of protein kinase clients upon Hsp90 inhibition. Our findings show that protein kinase clients Akt and Cdk4 are still degraded in mouse Ubr1(-)/(-) cells treated with geldanamycin, but that their levels recover much more rapidly than is found in wild type cells. These findings correlate with increased induction of Hsp90 expression in the...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313249</comments>
            <pubDate>Thu, 29 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313249</guid>        </item>
        <item>
            <title>Synchronous protein cycling in batch cultures of the yeast Saccharomyces cerevisiae at log growth phase.</title>
            <link>http://www.medworm.com/index.php?rid=5313251&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21978910%26dopt%3DAbstract</link>
            <description>Authors: Romagnoli G, Cundari E, Negri R, Crescenzi M, Farina L, Giuliani A, Bianchi MM
    Abstract
    The assumption that cells are temporally organized systems, i.e. showing relevant dynamics of their state variables such as gene expression or protein and metabolite concentration, while tacitly given for granted at the molecular level, is not explicitly taken into account when interpreting biological experimental data. This conundrum stems from the (undemonstrated) assumption that a cell culture, the actual object of biological experimentation, is a population of billions of independent oscillators (cells) randomly experiencing different phases of their cycles and thus not producing relevant coordinated dynamics at the population level. Moreover the fact of considering reproductive cyc...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313251</comments>
            <pubDate>Sat, 24 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313251</guid>        </item>
        <item>
            <title>Intestinal development and differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=5313250&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21978911%26dopt%3DAbstract</link>
            <description>Authors: Noah TK, Donahue B, Shroyer NF
    Abstract
    In this review, we present an overview of intestinal development and cellular differentiation of the intestinal epithelium. The review is separated into two sections: Section one summarizes organogenesis of the small and large intestines, including endoderm and gut tube formation in early embryogenesis, villus morphogenesis, and crypt formation. Section two reviews cell fate specification and differentiation of each cell type within the intestinal epithelium. Growth factor and transcriptional networks that regulate these developmental processes are summarized.
    PMID: 21978911 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313250</comments>
            <pubDate>Sat, 24 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313250</guid>        </item>
        <item>
            <title>Spontaneous transformation of adult mesenchymal stem cells from cynomolgus macaques in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=5313252&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21963525%26dopt%3DAbstract</link>
            <description>Authors: Ren Z, Wang J, Zhu W, Guan Y, Zou C, Chen Z, Zhang YA
    Abstract
    Mesenchymal stem cells (MSCs) have shown potential clinical utility in cell therapy and tissue engineering, due to their ability to proliferate as well as to differentiate into multiple lineages, including osteogenic, adipogenic, and chondrogenic specifications. Therefore, it is crucial to assess the safety of MSCs while extensive expansion ex vivo is a prerequisite to obtain the cell numbers for cell transplantation. Here we show that MSCs derived from adult cynomolgus monkey can undergo spontaneous transformation following in vitro culture. In comparison with MSCs, the spontaneously transformed mesenchymal cells (TMCs) display significantly different growth pattern and morphology, reminiscent of the character...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5313252</comments>
            <pubDate>Thu, 22 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5313252</guid>        </item>
        <item>
            <title>RhoA-ROCK-Myosin pathway regulates morphological plasticity of cultured olfactory ensheathing cells.</title>
            <link>http://www.medworm.com/index.php?rid=5281380&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21946234%26dopt%3DAbstract</link>
            <description>Authors: Huang ZH, Wang Y, Yuan XB, He C
    Abstract
    Olfactory ensheathing cells (OECs) are glial cells in the olfactory system with morphological and functional plasticity. Cultured OECs have the flattened and process-bearing shape. Reversible changes have been found between these two morphological phenotypes. However, the molecular mechanism underlying the regulation of their morphological plasticity remains elusive. Using RhoA FRET biosensor, we found that the active RhoA signal mainly distributed in the lamellipodia and/or filopodia of OECs. Local disruption of these active RhoA distributions led to the morphological change from the flattened into process-bearing shape and promoted process outgrowth. Furthermore, RhoA pathway inhibitors, Toxin-B, C3, Y-27632 or over-expression of ...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5281380</comments>
            <pubDate>Sat, 17 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5281380</guid>        </item>
        <item>
            <title>PHD1 interacts with ATF4 and negatively regulates its transcriptional activity without prolyl hydroxylation.</title>
            <link>http://www.medworm.com/index.php?rid=5281379&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21951999%26dopt%3DAbstract</link>
            <description>Authors: Hiwatashi Y, Kanno K, Takasaki C, Goryo K, Sato T, Torii S, Sogawa K, Yasumoto KI
    Abstract
    Cellular response to hypoxia plays an important role in both circulatory and pulmonary diseases and cancer. Hypoxia-inducible factors (HIFs) are major transcription factors regulating the response to hypoxia. The α-subunits of HIFs are hydroxylated by members of the prolyl-4-hydroxylase domain (PHD) family, PHD1, PHD2, and PHD3, in an oxygen-dependent manner. Here, we report on the identification of ATF4 as a protein interacting with PHD1 as well as PHD3, but not with PHD2. The central region of ATF4 including the Zipper II domain, ODD domain and β-TrCP recognition motif were involved in the interaction with PHD1. Coexistence of PHD1 stabilized ATF4, as opposed to the destabilizati...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5281379</comments>
            <pubDate>Sat, 17 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5281379</guid>        </item>
        <item>
            <title>Desmosome dynamics in migrating epithelial cells requires the actin cytoskeleton.</title>
            <link>http://www.medworm.com/index.php?rid=5281381&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21945137%26dopt%3DAbstract</link>
            <description>In this study we established a cell culture model to examine the fate of desmosomal components during scratch wound migration. Desmosomes are rapidly assembled between epithelial cells at the lateral edges of migrating cells and structures are transported in a retrograde fashion while the structures become larger and mature. Desmosome assembly and dynamics in this system are dependent on the actin cytoskeleton prior to being associated with the keratin intermediate filament cytoskeleton. These studies extend our understanding of desmosome assembly and provide a system to examine desmosome assembly and dynamics during epithelial cell migration.
    PMID: 21945137 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5281381</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5281381</guid>        </item>
        <item>
            <title>U bodies respond to nutrient stress in Drosophila.</title>
            <link>http://www.medworm.com/index.php?rid=5281384&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21939654%26dopt%3DAbstract</link>
            <description>Authors: Buckingham M, Liu JL
    Abstract
    The neurodegenerative disease spinal muscular atrophy (SMA) is caused by mutation of the survival motor neuron 1 (SMN1) gene. Cytoplasmic SMN protein-containing granules, known as U snRNP bodies (U bodies), are thought to be responsible for the assembly and storage of small nuclear ribonucleoproteins (snRNPs) which are essential for pre-mRNA splicing. U bodies exhibit close association with cytoplasmic processing bodies (P bodies), which are involved in mRNA decay and translational repression. The close association of the U body and P body in Drosophila resemble that of the stress granule and P body in yeast and mammalian cells. However, it is unknown whether the U body is responsive to any stress. Using Drosophila oogenesis as a model, here w...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5281384</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5281384</guid>        </item>
        <item>
            <title>NUMB does not impair growth and differentiation status of experimental gliomas.</title>
            <link>http://www.medworm.com/index.php?rid=5281382&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21939656%26dopt%3DAbstract</link>
            <description>Authors: Euskirchen P, Skaftnesmo KO, Huszthy PC, Brekkå N, Bjerkvig R, Jacobs AH, Miletic H
    Abstract
    The cell fate determinant NUMB orchestrates asymmetric cell division in flies and mammals and has lately been suggested to have a tumor suppressor function in breast and lung cancer. Here, we studied NUMB in the context of malignant gliomas. We used ectopic expression of NUMB in order to inhibit proliferation and induce differentiation in glioma cells by alteration of Notch, Hedgehog and p53 signaling. We found that NUMB is consistently expressed in glioma biopsies with predominance of NUMB2/4 isoforms as determined by isoform-specific real-time PCR and Western blotting. Upon lentiviral overexpression, in vitro proliferation rate and the grade of differentiation as assessed by mor...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5281382</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5281382</guid>        </item>
        <item>
            <title>Cellular repressor of E1A-stimulated genes regulates vascular endothelial cell migration by The ILK/AKT/mTOR/VEGF(165) signaling pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5281383&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21939655%26dopt%3DAbstract</link>
            <description>This study clarified the role and mechanism of a new vascular homeostasis regulator, Cellular repressor of E1A-stimulated genes (CREG), in the migration of primary human umbilical vein endothelial cells (HUVECs). A wound healing assay and transwell migration model showed that upregulation of CREG expression induced HUVEC migration and it was positively correlated with the expression of vascular endothelial growth factor. Furthermore, wild type integrin-linked kinase reversed the poor mobility of CREG knock-down HUVECs; in contrast, kinase-dead integrin-linked kinase weakened the migration of HUVECs. We also studied the effect of CREG on HUVEC migration by the addition of an mTOR inhibitor, recombinant vascular endothelial growth factor(165), neutralizing antibody of vascular endothelial gr...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5281383</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5281383</guid>        </item>
        <item>
            <title>Long isoform of ErbB3 binding protein, p48, mediates protein kinase B/Akt-dependent HDM2 stabilization and nuclear localization.</title>
            <link>http://www.medworm.com/index.php?rid=5247293&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21930127%26dopt%3DAbstract</link>
            <description>Authors: Kim CK, Lee SB, Nguyen TL, Lee KH, Um SH, Kim J, Ahn JY
    Abstract
    p48 is a long isoform of the ErbB3 binding protein that has oncogenic functions including promotion of carcinogenesis and induction of malignant transformation through negative regulation of tumor suppressor p53. Here, we show that high level of p48 protein expression leads to enhance HDM2 phosphorylation by Akt and inhibits the self-ubiquitination of HDM2 by up-regulation of Akt activity, thereby promoting its protein stability. Moreover, p48 expression leads to accumulated nuclear localization of HDM2, whereas p48 depletion disturbs its nuclear localization. Hence, higher expression of p48 in cancer cells reduces p53 levels through modulation of HDM2 nuclear localization and protein stability via regulation...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247293</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247293</guid>        </item>
        <item>
            <title>Laminin-111 derived peptides AG73 and C16 regulate invadopodia activity of a human adenoid cystic carcinoma cell line.</title>
            <link>http://www.medworm.com/index.php?rid=5247298&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21924264%26dopt%3DAbstract</link>
            <description>Authors: Nascimento CF, de Siqueira AS, Pinheiro JJ, Freitas VM, Jaeger RG
    Abstract
    Adenoid cystic carcinoma is a frequently occurring malignant salivary gland neoplasm with high level of recurrence and distant metastasis long time after treatment. Metastatic tumor cells that actively migrate and invade surrounding tissues rely on invadopodia to degrade extracellular matrix (ECM) barriers. Invadopodia are actin-rich membrane protrusions that localize enzymes required for ECM degradation. Breakdown of ECM macromolecules releases fragments and bioactive peptides. We have already demonstrated that laminin-111 and its derived peptides regulate migration, invasion and protease activity of adenocarcinoma cells. Here we addressed the role of laminin-111 peptides AG73 and C16 in invadopodi...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247298</comments>
            <pubDate>Wed, 07 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247298</guid>        </item>
        <item>
            <title>Evidence for non-CpG methylation in mammals.</title>
            <link>http://www.medworm.com/index.php?rid=5247297&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21925168%26dopt%3DAbstract</link>
            <description>Authors: Yan J, Zierath JR, Barrès R
    Abstract
    In mammals, the existence of cytosine methylation on non-CpG sequences is controversial. Here, we adapted a LuminoMetric-based Assay (LUMA) to determine global non-CpG methylation levels in rodent and human tissues. We observed that &amp;lt;1% cytosines in non-CpG motifs were methylated in 3T3-L1 fibroblasts, whereas 7-13% cytosines in non-CpG motifs were methylated in mouse tissues or embryonic fibroblasts. Analysis of cytosine methylation in human, rat, and mouse tissues by bisulfite sequencing revealed non-CpG methylation levels up to 7.5% of all non-CpG cytosines. These levels dropped to 1.5% when a second round of PCR was performed prior to bisulfite sequencing, providing an explanation for the common underestimation of non-CpG methyl...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247297</comments>
            <pubDate>Wed, 07 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247297</guid>        </item>
        <item>
            <title>Epidermal growth factor receptor reactivation induced by E-prostanoid-3 receptor- and tumor necrosis factor-alpha-converting enzyme-dependent feedback exaggerates interleukin-8 production in airway cancer (NCI-H292) cells.</title>
            <link>http://www.medworm.com/index.php?rid=5247296&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21925169%26dopt%3DAbstract</link>
            <description>Authors: Kim S, Lewis C, Nadel JA
    Abstract
    Airway epithelial cancer cells produce increased amounts of the chemokine interleukin-8 (IL-8), inducing pro-tumor responses. Multiple stimuli induce airway epithelial IL-8 production epidermal growth factor receptor (EGFR) dependently, but the mechanisms that exaggerate IL-8 production in airway cancers remain unknown. Here we show that direct activation of EGFR (EGFR-P) by its ligand transforming growth factor (TGF)-alpha induces a second EGFR-P in human airway (NCI-H292) cancer cells but not in normal human bronchial epithelial (NHBE) cells, exaggerating IL-8 production in these cancer cells. The second EGFR-P in NCI-H292 cells was caused by metalloprotease TNF-alpha-converting enzyme (TACE)-dependent cleavage of EGFR pro-ligands and wa...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247296</comments>
            <pubDate>Wed, 07 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247296</guid>        </item>
        <item>
            <title>GADD34 mediates cytoprotective autophagy in mutant huntingtin expressing cells via the mTOR pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5247295&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21925170%26dopt%3DAbstract</link>
            <description>Authors: Hyrskyluoto A, Reijonen S, Kivinen J, Lindholm D, Korhonen L
    Abstract
    Increased protein aggregation and altered cell signaling accompany many neurodegenerative diseases including Huntington's disease (HD). Cell stress is counterbalanced by signals mediating cell repair but the identity of these are not fully understood. We show here that the mammalian target of rapamycin (mTOR) pathway is inhibited and cytoprotective autophagy is activated in neuronal PC6.3 cells at 24h after expression of mutant huntingtin proteins. Tuberous sclerosis complex (TSC) 1/2 interacted with growth arrest and DNA damage protein 34 (GADD34), which caused TSC2 dephosphorylation and induction of autophagy in mutant huntingtin expressing cells. However, GADD34 and autophagy decreased at later time p...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247295</comments>
            <pubDate>Wed, 07 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247295</guid>        </item>
        <item>
            <title>EGFR-targeted therapy.</title>
            <link>http://www.medworm.com/index.php?rid=5247294&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21925171%26dopt%3DAbstract</link>
            <description>Authors: Vecchione L, Jacobs B, Normanno N, Ciardiello F, Tejpar S
    Abstract
    Anti-Epidermal Growth Factor Receptor (EGFR) therapies have been recently developed for the treatment of multiple cancer types. At the time when they were introduced in clinical practice, there was little knowledge of the molecular bases of tumor sensitivity and resistance to these novel targeted compounds. By using the framework of anti-EGFR inhibitors as treatment for colorectal cancer patients, we will review the knowledge we have reached until now in improving the development of a personalized cancer therapy and we will try to indicate the future challenges this field will face in the future.
    PMID: 21925171 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247294</comments>
            <pubDate>Wed, 07 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247294</guid>        </item>
        <item>
            <title>Hepatocyte-derived cultured cells with unusual cytoplasmic keratin-rich spheroid bodies.</title>
            <link>http://www.medworm.com/index.php?rid=5219231&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21907707%26dopt%3DAbstract</link>
            <description>In conclusion, our data suggest that Huh-7w7.3 cells constitute an excellent model for determining the cellular factor(s) involved in the process of spheroid perinuclear body formation.
    PMID: 21907707 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5219231</comments>
            <pubDate>Wed, 31 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5219231</guid>        </item>
        <item>
            <title>The origin of pre-neoplastic metaplasia in the stomach: Chief cells emerge from the Mist.</title>
            <link>http://www.medworm.com/index.php?rid=5219230&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21907708%26dopt%3DAbstract</link>
            <description>Authors: Goldenring JR, Nam KT, Mills JC
    Abstract
    The digestive-enzyme secreting, gastric epithelial chief (zymogenic) cell is remarkable and underappreciated. Here, we discuss how all available evidence suggests that mature chief cells in the adult, mammalian stomach are postmitotic, slowly turning over cells that arise via a relatively long-lived progenitor, the mucous neck cell, The differentiation of chief cells from neck cells does not involve cell division, and the neck cell has its own distinct pattern of gene expression and putative physiological function. Thus, the ontogeny of the normal chief cell lineage exemplifies transdifferentiation. Furthermore, under pathophysiogical loss of acid-secreting parietal cell, the chief cell lineage can itself trasndifferentiate into a m...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5219230</comments>
            <pubDate>Wed, 31 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5219230</guid>        </item>
        <item>
            <title>Effects of SDF-1-CXCR4 signaling on microRNA expression and tumorigenesis in estrogen receptor-alpha (ER-α)-positive breast cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5219233&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21906588%26dopt%3DAbstract</link>
            <description>Authors: Rhodes LV, Bratton MR, Zhu Y, Tilghman SL, Muir SE, Salvo VA, Tate CR, Elliott S, Nephew KP, Collins-Burow BM, Burow ME
    Abstract
    The majority of breast cancer cases ultimately become unresponsive to endocrine therapies, and this progression of breast cancer from hormone-responsive to hormone-independent represents an area in need of further research. Additionally, hormone-independent carcinomas are characterized as being more aggressive and metastatic, key features of more advanced disease. Having previously shown the ability of the stromal-cell derived factor-1 (SDF-1)-CXCR4 signaling axis to promote primary tumorigenesis and hormone independence by overexpressing CXCR4 in MCF-7 cells, in this study we further examined the role of SDF-1/CXCR4 in the endogenously CXCR4-pos...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5219233</comments>
            <pubDate>Tue, 30 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5219233</guid>        </item>
        <item>
            <title>Caspase-8, c-FLIP, and caspase-9 in c-Myc-induced apoptosis of fibroblasts.</title>
            <link>http://www.medworm.com/index.php?rid=5219234&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21903094%26dopt%3DAbstract</link>
            <description>Authors: Järvinen K, Hotti A, Santos L, Nummela P, Hölttä E
    Abstract
    c-Myc is known to induce or potentiate apoptotic processes predominantly by triggering or enhancing the activity of caspases, but the activation mechanisms of caspases by c-Myc remain still poorly understood. Here we found that in MycER™ rat fibroblasts the activation of c-Myc led to an early activation and cleavage of the initiator caspase-8, and concurrent processing and activation of the effector caspases 3 and 7. Interestingly, the expression of cellular FLICE inhibitory protein (c-FLIP) mRNA and the encoded protein, c-FLIP(L), a catalytically inactive homologue of caspase-8, were down-regulated prior to or coincidently with the activation of caspase-8. Of the other known initiators, caspase-9, involved i...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5219234</comments>
            <pubDate>Sun, 28 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5219234</guid>        </item>
        <item>
            <title>Nanobody-based chimeric receptor gene integration in Jurkat cells mediated by PhiC31 integrase.</title>
            <link>http://www.medworm.com/index.php?rid=5219232&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21906589%26dopt%3DAbstract</link>
            <description>Authors: Iri-Sofla FJ, Rahbarizadeh F, Ahmadvand D, Rasaee MJ
    Abstract
    The crucial role of T lymphocytes in anti-tumor immunity has led to the development of novel strategies that can target and activate T cells against tumor cells. Recombinant DNA technology has been used to generate non-MHC-restricted chimeric antigen receptors (CARs). Here, we constructed a panel of recombinant CAR that harbors the anti-MUC1 nanobody and the signaling and co-signaling moieties (CD3ζ/CD28) with different spacer regions derived from human IgG3 with one or two repeats of the hinge sequence or the hinge region of FcγRII. The PhiC31 integrase system was employed to investigate if the recombination efficiency could be recruited for high and stable expression of T cell chimeric receptor genes. The ef...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5219232</comments>
            <pubDate>Sun, 28 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5219232</guid>        </item>
        <item>
            <title>The subpopulation of mesenchymal stem cells that differentiate toward cardiomyocytes is cardiac progenitor cells.</title>
            <link>http://www.medworm.com/index.php?rid=5193042&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21878326%26dopt%3DAbstract</link>
            <description>Authors: Wei F, Wang T, Liu J, Du Y, Ma A
    Abstract
    Mesenchymal stem cells (MSCs) are regarded as a promising source of cell-based therapy for heart injury. In fact, less than 30% of MSCs contribute to cardiomyocytes differentiation, and the isolation procedure and biological characteristics of this population of cells remain unknown. Here we isolate and investigate the biological characteristics of this subpopulation of MSCs. Twenty four MSC clones were randomly selected using single-cell monoclonal technology. After induced with 5-azacytidine, eight clones displayed cardiomyocyte-like morphologies, and highly (over 90%) expressed cardiac-specific markers cTnT and α-actin, and displayed transient outward K(+) current (I(to)), inwardly rectifying K(+) current (I(K1)) and delayed re...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5193042</comments>
            <pubDate>Sun, 21 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5193042</guid>        </item>
        <item>
            <title>Wnt signaling and colon tumorigenesis - A view from the periphery.</title>
            <link>http://www.medworm.com/index.php?rid=5193041&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21884696%26dopt%3DAbstract</link>
            <description>Authors: Burgess AW, Faux MC, Layton MJ, Ramsay RG
    Abstract
    In this brief overview we discuss the association between Wnt signaling and colon cell biology and tumorigenesis. Our current understanding of the role of Apc in the β-catenin destruction complex is compared with potential roles for Apc in cell adhesion and migration. The requirement for phosphorylation in the proteasomal-mediated degradation of β-catenin is contrasted with roles for phospho-β-catenin in the activation of transcription, cell adhesion and migration. The synergy between Myb and β-catenin regulation of transcription in crypt stem cells during Wnt signaling is discussed. Finally, potential effects of growth factor regulatory systems, Apc or truncated-Apc on crypt morphogenesis, stem cell localization and c...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5193041</comments>
            <pubDate>Sun, 21 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5193041</guid>        </item>
        <item>
            <title>Focal adhesion protein abnormalities in myelodysplastic mesenchymal stromal cells.</title>
            <link>http://www.medworm.com/index.php?rid=5193046&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21871449%26dopt%3DAbstract</link>
            <description>Authors: Aanei CM, Eloae FZ, Flandrin P, Tavernier E, Carasevici E, Guyotat D, Campos L
    Abstract
    Direct cell-cell contact between haematopoietic progenitor cells (HPCs) and their cellular microenvironment is essential to maintain 'stemness'. In cancer biology, focal adhesion (FA) proteins are involved in survival signal transduction in a wide variety of human tumours. To define the role of FA proteins in the haematopoietic microenvironment of myelodysplastic syndromes (MDS), CD73-positive mesenchymal stromal cells (MSCs) were immunostained for paxillin, pFAK [Y(397)], and HSP90α/β and p130CAS, and analysed for reactivity, intensity and cellular localisation. Immunofluorescence microscopy allowed us to identify qualitative and quantitative differences, and subcellular localisation...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5193046</comments>
            <pubDate>Mon, 15 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5193046</guid>        </item>
        <item>
            <title>Lamin A, farnesylation and aging.</title>
            <link>http://www.medworm.com/index.php?rid=5193045&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21871450%26dopt%3DAbstract</link>
            <description>Authors: Reddy S, Comai L
    Abstract
    Lamin A is a component of the nuclear envelope that is synthesized as a precursor prelamin A molecule and then processed into mature lamin A through sequential steps of posttranslational modifications and proteolytic cleavages. Remarkably, over 400 distinct point mutations have been so far identified throughout the LMNA gene, which result in the development of at least ten distinct human disorders, collectively known as laminopathies, among which is the premature aging disease Hutchinson-Gilford progeria syndrome (HGPS). The majority of HGPS cases are associated with a single point mutation in the LMNA gene that causes the production of a permanently farnesylated mutant lamin A protein termed progerin. The mechanism by which progerin leads to prem...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5193045</comments>
            <pubDate>Mon, 15 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5193045</guid>        </item>
        <item>
            <title>Human STEAP3 maintains tumor growth under hypoferric condition.</title>
            <link>http://www.medworm.com/index.php?rid=5193044&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21871451%26dopt%3DAbstract</link>
            <description>Authors: Isobe T, Baba E, Arita S, Komoda M, Tamura S, Shirakawa T, Ariyama H, Takaishi S, Kusaba H, Ueki T, Akashi K
    Abstract
    Iron is essential in cellular proliferation and survival based on its crucial roles in DNA and ATP synthesis. Tumor cells proliferate rapidly even in patients with low serum iron, although their actual mechanisms are not well known. To elucidate molecular mechanisms of efficient tumor progression under the hypoferric condition, we studied the roles of six-transmembrane epithelial antigen of the prostate family member 3 (STEAP3), which was reported to facilitate iron uptake. Using Raji cells with low STEAP3 mRNA expression, human STEAP3-overexpressing cells were established. The impact of STEAP3 expression was analyzed about the amount of iron storage, the s...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5193044</comments>
            <pubDate>Mon, 15 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5193044</guid>        </item>
        <item>
            <title>The Raf/MEK/extracellular signal-regulated kinase 1/2 pathway can mediate growth inhibitory and differentiation signaling via androgen receptor downregulation in prostate cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5193043&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21871886%26dopt%3DAbstract</link>
            <description>Authors: Hong SK, Kim JH, Lin MF, Park JI
    Abstract
    Upregulated ERK1/2 activity is correlated with androgen receptor (AR) downregulation in certain prostate cancer (PCa) that exhibits androgen deprivation-induced neuroendocrine differentiation, but its functional relevance requires elucidation. We found that sustained ERK1/2 activation using active Raf or MEK1/2 mutants is sufficient to induce AR downregulation at mRNA and protein levels in LNCaP. Downregulation of AR protein, but not mRNA, was blocked by proteasome inhibitors, MG132 and bortezomib, indicating that the pathway regulation is mediated at multiple points. Ectopic expression of a constitutively active AR inhibited Raf/MEK/ERK-mediated regulation of the differentiation markers, neuron-specific enolase and neutral endopep...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5193043</comments>
            <pubDate>Mon, 15 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5193043</guid>        </item>
        <item>
            <title>Mammalian ChlR1 has a role in heterochromatin organization.</title>
            <link>http://www.medworm.com/index.php?rid=5157501&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21854770%26dopt%3DAbstract</link>
            <description>In this study, we show that human ChlR1 deficient cells exhibit abnormal heterochromatin organization. While constitutive heterochromatin is discretely localized at perinuclear and perinucleolar regions in control HeLa cells, ChlR1-depleted cells showed dispersed localization of constitutive heterochromatin accompanied by disrupted centromere clustering. Cells isolated from Ddx11(-/-) embryos also exhibited diffuse localization of centromeres and heterochromatin foci. Similar abnormalities were found in HeLa cells depleted of combinations of HP1α and HP1β. Immunofluorescence and chromatin immunoprecipitation showed a decreased level of HP1α at pericentric regions in ChlR1-depleted cells. Trimethyl-histone H3 at lysine 9 (H3K9-me3) was also modestly decreased at pericentric sequences. Th...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157501</comments>
            <pubDate>Wed, 10 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157501</guid>        </item>
        <item>
            <title>Intestinal stem cells in the adult Drosophila midgut.</title>
            <link>http://www.medworm.com/index.php?rid=5157499&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21856297%26dopt%3DAbstract</link>
            <description>Authors: Jiang H, Edgar BA
    Abstract
    Drosophila has long been an excellent model organism for studying stem cell biology. Notably, studies of Drosophila's germline stem cells have been instrumental in developing the stem cell niche concept. The recent discovery of somatic stem cells in adult Drosophila, particularly the intestinal stem cells (ISCs) of the midgut, has established Drosophila as an exciting model to study stem cell-mediated adult tissue homeostasis and regeneration. Here, we review the major signaling pathways that regulate the self-renewal, proliferation and differentiation of Drosophila ISCs, discussing how this regulation maintains midgut homeostasis and mediates regeneration of the intestinal epithelium after injury.
    PMID: 21856297 [PubMed - as supplied by publ...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157499</comments>
            <pubDate>Wed, 10 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157499</guid>        </item>
        <item>
            <title>Fibroblasts from the muscles of Duchenne muscular dystrophy patients are resistant to cell detachment apoptosis.</title>
            <link>http://www.medworm.com/index.php?rid=5157508&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21851816%26dopt%3DAbstract</link>
            <description>Authors: Zanotti S, Gibertini S, Bragato C, Mantegazza R, Morandi L, Mora M
    Abstract
    Extracellular matrix (ECM) proteins, including collagen and growth factors, are greatly increased in tissue fibrosis and mainly secreted by fibroblasts. We previously demonstrated that muscle-derived fibroblasts from Duchenne muscular dystrophy (DMD) patients have a profibrotic phenotype, that includes significantly reduced expression of tissue inhibitor of metalloprotease 3 (TIMP-3) compared to control. Since TIMP-3 induces apoptosis in various cell types, we hypothesized increased resistance of DMD fibroblasts to apoptosis. To address this, we evaluated apoptotic nuclei, caspase 3, caspase 3 substrate expression, and migration and adhesion properties of muscle-derived fibroblasts, after applying ...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157508</comments>
            <pubDate>Mon, 08 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157508</guid>        </item>
        <item>
            <title>α1-Adrenergic drugs exhibit affinity to a thapsigargin-sensitive binding site and interfere with the intracellular Ca(2+) homeostasis in human erythroleukemia cells.</title>
            <link>http://www.medworm.com/index.php?rid=5157505&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21851819%26dopt%3DAbstract</link>
            <description>Authors: Fuchs R, Schraml E, Leitinger G, Letofsky-Papst I, Stelzer I, Haas HS, Schauenstein K, Sadjak A
    Abstract
    Even though the erythroleukemia cell lines K562 and HEL do not express α1-adrenoceptors, some α1-adrenergic drugs influence both survival and differentiation of these cell lines. Since Ca(2+) is closely related to cellular homeostasis, we examined the capacity of α1-adrenergic drugs to modulate the intracellular Ca(2+) content in K562 cells. Because of morphological alterations of mitochondria following α1-adrenergic agonist treatment, we also scrutinized mitochondrial functions. In order to visualize the non-adrenoceptor binding site(s) of α1-adrenergic drugs in erythroleukemia cells, we evaluated the application of the fluorescent α1-adrenergic antagonist BODIPY...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157505</comments>
            <pubDate>Mon, 08 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157505</guid>        </item>
        <item>
            <title>Acrolein sensitizes human renal cancer Caki cells to TRAIL-induced apoptosis via ROS-mediated up-regulation of death receptor-5 (DR5) and down-regulation of Bcl-2.</title>
            <link>http://www.medworm.com/index.php?rid=5157503&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21854768%26dopt%3DAbstract</link>
            <description>Authors: Yang ES, Woo SM, Choi KS, Kwon TK
    Abstract
    TRAIL resistance in many cancer cells is one of the major problems in TRAIL-based cancer therapy. Thus, the agents that can sensitize the tumor cells to TRAIL-mediated apoptosis are strictly needed for the improvement of anti-cancer effect of TRAIL. Acrolein is a byproduct of lipid peroxidation, which has been involved in pulmonary, cardiac and neurodegenerative diseases. We investigated whether acrolein, an α,β-unsaturated aldehyde, can potentiate TRAIL-induced apoptosis in human renal cancer cells. The combined treatment with acrolein and TRAIL significantly induced apoptosis, and stimulated of caspase-3 activity, DNA fragmentation, and cleavage of PARP. We found that acrolein down-regulated the protein level of Bcl-2 and Bcl-...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157503</comments>
            <pubDate>Mon, 08 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157503</guid>        </item>
        <item>
            <title>Mechanical stretch augments insulin-induced vascular smooth muscle cell proliferation by insulin-like growth factor-1 receptor.</title>
            <link>http://www.medworm.com/index.php?rid=5157502&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21854769%26dopt%3DAbstract</link>
            <description>Authors: Liu G, Hitomi H, Hosomi N, Lei B, Nakano D, Deguchi K, Mori H, Masaki T, Ma H, Griendling KK, Nishiyama A
    Abstract
    Insulin resistance and hypertension have been implicated in the pathogenesis of cardiovascular disease; however, little is known about the roles of insulin and mechanical force in vascular smooth muscle cell (VSMC) remodeling. We investigated the contribution of mechanical stretch to insulin-induced VSMC proliferation. Thymidine incorporation was stimulated by insulin in stretched VSMCs, but not in un-stretched VSMCs. Insulin increased 2-deoxy-glucose incorporation in both stretched and un-stretched VSMCs. Mechanical stretch augmented insulin-induced extracellular signal-regulated kinase (ERK) and Akt phosphorylation. Inhibitors of epidermal growth factor (EGF...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157502</comments>
            <pubDate>Mon, 08 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157502</guid>        </item>
        <item>
            <title>N-cadherin mediates angiogenesis by regulating monocyte chemoattractant protein-1 expression via PI3K/Akt signaling in prostate cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5157500&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21855541%26dopt%3DAbstract</link>
            <description>Authors: Nalla AK, Estes N, Patel J, Rao JS
    Abstract
    Over the past decade, evidence continues to mount showing that N-cadherin is a critical protein in cancer progression and metastasis. In the present study, we evaluated the expression of N-cadherin in human prostate cancer tissue specimens and cell lines. Enhanced expression of N-cadherin was observed in both the malignant and bone-metastasized prostate tissue specimens compared to the healthy prostate tissues. Consistent with the tissue data, N-cadherin was highly expressed in PC3, but not in Du145 and LNCaP human prostate cell lines. Based on cell to cell binding assay, we found that N-cadherin expression facilitates homotypic interaction between human prostate cancer cells and human microvascular endothelial cells (HMEC). Huma...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157500</comments>
            <pubDate>Mon, 08 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157500</guid>        </item>
        <item>
            <title>The lipid kinase PI4KIIIβ and the eEF1A2 oncogene co-operate to disrupt three-dimensional in vitro acinar morphogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5157507&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21851817%26dopt%3DAbstract</link>
            <description>In this report, we find that phosphatidylinositol 4-kinase IIIβ (PI4KIIIβ), a lipid kinase that phosphorylates phosphatidylinositol (PI) to PI(4)P, disrupts in vitro mammary acinar formation. The PI4KIIIβ protein localizes to the basal surface of acini created by human MCF10A cells and ectopic expression of PI4KIIIβ induces multi-acinar devlopment. Furthermore, expression of an oncogenic PI4KIIIβ activator, eEF1A2 (eukaryotic elongation factor 1 alpha 2), phenocopies the PI4KIIIβ multi-acinar phenotype. Ectopic expression of PI4KIIIβ or eEF1A2 alters the localization of PI(4)P and PI(4,5)P(2) within acini, indicating the importance of these lipids in acinar development. Our work shows that PI4KIIIβ, eEF1A2 and PI(4)P likely play an important role in mammary neoplasia and acinar dev...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157507</comments>
            <pubDate>Sat, 06 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157507</guid>        </item>
        <item>
            <title>Wnt/Myc interactions in intestinal cancer: Partners in crime.</title>
            <link>http://www.medworm.com/index.php?rid=5157506&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21851818%26dopt%3DAbstract</link>
            <description>Authors: Myant K, Sansom OJ
    Abstract
    Loss of the APC (adenomatous polyposis coli) gene in colorectal cancer leads to a rapid deregulation of TCF/LEF target genes. Of all these target genes, the transcription factor c-MYC appears the most critical. In this review we will discuss the interplay of Wnt and c-MYC signaling during intestinal homeostasis and transformation. Furthermore, we will discuss recent data showing that further deregulation of c-MYC levels during colorectal carcinogenesis may drive tumor progression. Moreover, understanding these additional control mechanisms may allow targeting of c-MYC during colorectal carcinogenesis.
    PMID: 21851818 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157506</comments>
            <pubDate>Sat, 06 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157506</guid>        </item>
        <item>
            <title>MUC6 mucin expression inhibits tumor cell invasion.</title>
            <link>http://www.medworm.com/index.php?rid=5157504&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21851820%26dopt%3DAbstract</link>
            <description>Authors: Leir SH, Harris A
    Abstract
    The MUC6 mucin has a critical protective function in the normal stomach, pancreas and duodenum and is aberrantly expressed during the progression of some gastrointestinal cancers. Our aim was to determine whether MUC6 contributes to the etiology or progression of pancreatic cancer and elucidate the molecular basis of its involvement. Expression of MUC6 glycoprotein was examined in pancreatic cancer tissues by immunofluorescence and loss of MUC6 was observed. Next, to determine whether MUC6 inhibits tumor growth and metastasis by altering cell adhesion and invasion, recombinant MUC6 cDNA and separate MUC6 N-terminal and C-terminal domains were transfected into pancreatic, colorectal and breast cancer cell lines. The recombinant N- and C-terminal p...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157504</comments>
            <pubDate>Thu, 04 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157504</guid>        </item>
        <item>
            <title>Conserved signaling through vascular endothelial growth (VEGF) receptor family members in murine lymphatic endothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=5141601&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21839079%26dopt%3DAbstract</link>
            <description>We describe a robust protocol for isolation of mLECs which, by harnessing the power of transgenic and knockout mouse models, will be a useful tool to study how LEC phenotype contributes to alterations in lymphatic vessel formation and function.
    PMID: 21839079 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141601</comments>
            <pubDate>Mon, 01 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141601</guid>        </item>
        <item>
            <title>Accumulation of Ku70 at DNA double-strand breaks in living epithelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=5141607&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21820429%26dopt%3DAbstract</link>
            <description>Authors: Koike M, Yutoku Y, Koike A
    Abstract
    Ku70 and Ku80 play an essential role in the DNA double-strand break (DSB) repair pathway, i.e., nonhomologous DNA-end-joining (NHEJ). No accumulation mechanisms of Ku70 at DSBs have been clarified in detail, although the accumulation mechanism of Ku70 at DSBs plays key roles in regulating the NHEJ activity. Here, we show the essential domains for the accumulation and function of Ku70 at DSBs in living lung epithelial cells. Our results showed that EGFP-Ku70 accumulation at DSBs began immediately after irradiation. Our findings demonstrate that three domains of Ku70, i.e., the α/β, DNA-binding, and Ku80-binding domains, but not the SAP domain, are necessary for the accumulation at or recognition of DSBs in the early stage after irradiat...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141607</comments>
            <pubDate>Thu, 28 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141607</guid>        </item>
        <item>
            <title>The intracellular domain of Jagged-1 interacts with Notch1 intracellular domain and promotes its degradation through Fbw7 E3 ligase.</title>
            <link>http://www.medworm.com/index.php?rid=5141606&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21820430%26dopt%3DAbstract</link>
            <description>In this study, we have demonstrated that the Jagged-1 intracellular domain (JICD) inhibits Notch1 signaling via a reduction in the protein stability of the Notch1 intracellular domain (Notch1-IC). The formation of the Notch1-IC-RBP-Jk-Mastermind complex is prevented in the presence of JICD, via a physical interaction. Furthermore, JICD accelerates the protein degradation of Notch1-IC via Fbw7-dependent proteasomal pathway. These results indicate that JICD functions as a negative regulator in Notch1 signaling via the promotion of Notch1-IC degradation.
    PMID: 21820430 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141606</comments>
            <pubDate>Thu, 28 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141606</guid>        </item>
        <item>
            <title>Control of cell adhesion and compartmentalization in the intestinal epithelium.</title>
            <link>http://www.medworm.com/index.php?rid=5141605&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21820431%26dopt%3DAbstract</link>
            <description>Authors: Solanas G, Batlle E
    Abstract
    Continuous cell renewal in the intestinal mucosa occurs without disrupting the integrity of the epithelial layer. Despite the restrictions imposed by strong cell-to-cell adhesions, epithelial intestinal cells migrate constantly between tissue compartments. Alterations in cell adhesion and compartmentalization play key roles in diseases of the intestine. In particular, decreased E-cadherin-mediated adhesion during inflammatory bowel disease and loss of EphB/ephrin-B-mediated compartmentalization in colorectal cancer have recently emerged as key players of these prevalent pathologies. Here we will review our current knowledge on how cell-to-cell adhesion, migration and cell positioning are coordinated in the intestinal epithelium. We will highlig...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141605</comments>
            <pubDate>Thu, 28 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141605</guid>        </item>
        <item>
            <title>Plectin regulates invasiveness of SW480 colon carcinoma cells and is targeted to podosome-like adhesions in an isoform-specific manner.</title>
            <link>http://www.medworm.com/index.php?rid=5141604&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21821021%26dopt%3DAbstract</link>
            <description>Authors: McInroy L, Määttä A
    Abstract
    Co-ordination of cytoskeletal networks and their dynamics is an essential feature of cell migration and cancer cell invasion. Plectin is a large cytolinker protein that influences tissue integrity, organisation of actin and intermediate filaments, and cell migration. Alternatively spliced plectin isoforms are targeted to different subcellular locations. Here, we show that plectin ablation by siRNA impaired migration, invasion and adhesion of SW480 colon carcinoma cells. A previously less well characterised plectin isoform, plectin-1k, co-localised with epithelial integrins, N-WASP, cortactin, and dynamin in podosome-like adhesions in invasive SW480 colon carcinoma cells. Transfection of alternative plectin N-terminal constructs demonstrated ...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141604</comments>
            <pubDate>Thu, 28 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141604</guid>        </item>
        <item>
            <title>Mechanotransduction activates α(5)β(1) integrin and PI3K/Akt signaling pathways in mandibular osteoblasts.</title>
            <link>http://www.medworm.com/index.php?rid=5141603&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21824471%26dopt%3DAbstract</link>
            <description>Authors: Watabe H, Furuhama T, Tani-Ishii N, Mikuni-Takagaki Y
    Abstract
    It is unclear how bone cells at different sites detect mechanical loading and how site-specific mechanotransduction affects bone homeostasis. To differentiate the anabolic mechanical responses of mandibular cells from those of calvarial and long bone cells, we isolated osteoblasts from C57B6J mouse bones, cultured them for 1week, and subjected them to therapeutic low intensity pulsed ultrasound (LIPUS). While the expression of the marker proteins of osteoblasts and osteocytes such as alkaline phosphatase and FGF23, as well as Wnt1 and β-catenin, was equally upregulated, the expression of mandibular osteoblast messages related to bone remodeling and apoptosis differed from that of messages of other osteoblasts,...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141603</comments>
            <pubDate>Thu, 28 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141603</guid>        </item>
        <item>
            <title>Prosaposin sorting is mediated by oligomerization.</title>
            <link>http://www.medworm.com/index.php?rid=5141602&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21835174%26dopt%3DAbstract</link>
            <description>In conclusion, we are reporting for the first time that oligomerization of prosaposin is crucial for its entry into the secretory pathway.
    PMID: 21835174 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141602</comments>
            <pubDate>Thu, 28 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141602</guid>        </item>
        <item>
            <title>TCTP is a critical survival factor that protects cancer cells from oxidative stress-induced cell-death.</title>
            <link>http://www.medworm.com/index.php?rid=5103956&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21801721%26dopt%3DAbstract</link>
            <description>Authors: Lucibello M, Gambacurta A, Zonfrillo M, Pierimarchi P, Serafino A, Rasi G, Rubartelli A, Garaci E
    The translationally controlled tumor protein (TCTP) displays growth-promoting and antiapoptotic properties. To gain information on the role of TCTP in cancer disease, we studied the modulation of TCTP and cell survival under stress conditions on tumor cell lines of different origins. When cancer cells were exposed to a mild oxidative stress, such low doses of Arsenic trioxide (ATO) or hydrogen peroxide (H(2)O(2)), up-regulation of TCTP was observed in cells survived to the treatment. Differently, a strong oxidative hit provided by ATO combined with glutathione (GSH) depletion or condition of glucose deprivation caused a down-modulation of TCTP followed by cell death. Clones with a...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103956</comments>
            <pubDate>Fri, 22 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103956</guid>        </item>
        <item>
            <title>Boundaries, junctions and transitions in the gastrointestinal tract.</title>
            <link>http://www.medworm.com/index.php?rid=5103955&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21802415%26dopt%3DAbstract</link>
            <description>Authors: San Roman AK, Shivdasani RA
    Contiguous regions along the mammalian gastrointestinal tract, from the esophagus to the rectum, serve distinct digestive functions. Some organs, such as the esophagus and glandular stomach or the small bowel and colon, are separated by sharp boundaries. The duodenal, jejunal and ileal segments of the small intestine, by contrast, have imprecise borders. Because human esophageal and gastric cancers frequently arise in a background of tissue metaplasia and some intestinal disorders are confined to discrete regions, it is useful to appreciate the molecular and cellular basis of boundary formation and preservation. Here we review the anatomy and determinants of boundaries and transitions in the alimentary canal with respect to tissue morphology, gene e...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103955</comments>
            <pubDate>Fri, 22 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103955</guid>        </item>
        <item>
            <title>Role of aquaporins in cell migration and edema formation in human brain tumors.</title>
            <link>http://www.medworm.com/index.php?rid=5103960&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21784068%26dopt%3DAbstract</link>
            <description>Authors: Nico B, Ribatti D
    The aquaporins (AQPs) are a family of transmembrane water channel proteins widely distributed and play a major role in transcellular and transepithelial water movement. Moreover, recent evidence indicates that AQPs may be involved in cell migration, angiogenesis, and tumor growth. This review article summarizes literature data concerning the involvement of AQP-1 and -4 in human brain tumor growth and edema formation and suggests a potential therapeutic approach by antagonizing their biological activity.
    PMID: 21784068 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103960</comments>
            <pubDate>Wed, 20 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103960</guid>        </item>
        <item>
            <title>Hepatic response to aluminum toxicity: Dyslipidemia and liver diseases.</title>
            <link>http://www.medworm.com/index.php?rid=5103959&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21787768%26dopt%3DAbstract</link>
            <description>Authors: Mailloux RJ, Lemire J, Appanna VD
    Aluminum (Al) is a metal toxin that has been implicated in the etiology of a number of diseases including Alzheimer's, Parkinson's, dialysis encephalopathy, and osteomalacia. Al has been shown to exert its effects by disrupting lipid membrane fluidity, perturbing iron (Fe), magnesium, and calcium homeostasis, and causing oxidative stress. However, the exact molecular targets of aluminum's toxicity have remained elusive. In the present review, we describe how the use of a systems biology approach in cultured hepatoblastoma cells (HepG2) allowed the identification of the molecular targets of Al toxicity. Mitochondrial metabolism is the main site of the toxicological action of Al. Fe-dependent and redox sensitive enzymes in the tricarboxylic acid...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103959</comments>
            <pubDate>Tue, 19 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103959</guid>        </item>
        <item>
            <title>Stem cell self-renewal in intestinal crypt.</title>
            <link>http://www.medworm.com/index.php?rid=5103958&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21787769%26dopt%3DAbstract</link>
            <description>Authors: Simons BD, Clevers H
    As a rapidly cycling tissue capable of fast repair and regeneration, the intestinal epithelium has emerged as a favored model system to explore the principles of adult stem cell biology. However, until recently, the identity and characteristics of the stem cell population in both the small intestine and colon has remained the subject of debate. Recent studies based on targeted lineage tracing strategies, combined with the development of an organotypic culture system, have identified the crypt base columnar cell as the intestinal stem cell, and have unveiled the strategy by which the balance between proliferation and differentiation is maintained. These results show that intestinal stem cells operate in a dynamic environment in which frequent and stochastic...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103958</comments>
            <pubDate>Tue, 19 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103958</guid>        </item>
        <item>
            <title>Regulation of ciliary beat frequency by the nitric oxide signaling pathway in mouse nasal and tracheal epithelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=5103957&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21787770%26dopt%3DAbstract</link>
            <description>CONCLUSION: NO plays a role in regulating CBF of mouse respiratory epithelial cells via a eNOS-NO-sGC β-cGMP-PKG I pathway.
    PMID: 21787770 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5103957</comments>
            <pubDate>Tue, 19 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5103957</guid>        </item>
        <item>
            <title>Evidence that phosphorylation by the mitotic kinase Cdk1 promotes ICER monoubiquitination and nuclear delocalization.</title>
            <link>http://www.medworm.com/index.php?rid=5058050&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21767532%26dopt%3DAbstract</link>
            <description>In this report data is presented demonstrating that ICER is phosphorylated by the mitotic kinase cdk1. Phosphorylation of ICER on a discrete residue targeted ICER to be monoubiquitinated. Differently that unphosphorylated, phosphorylated and polyubiquitinated ICER, monoubiquitinated ICER was found to be cytosolic. Taken together, these results hinted on a mechanism for the observed abnormal subcellular localization of ICER in human prostate tumors.
    PMID: 21767532 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5058050</comments>
            <pubDate>Thu, 14 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5058050</guid>        </item>
        <item>
            <title>Impaired response of mature adipocytes of diabetic mice to hypoxia.</title>
            <link>http://www.medworm.com/index.php?rid=5058049&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21777581%26dopt%3DAbstract</link>
            <description>In this study, we established a novel in vitro culture method of mature adipocytes by enclosing them in a hyaluronan (HA) based hydrogel to study their role in response to stress such as hypoxia. BrdU labeling and Ki67 immunostaining experiments showed that hydrogel enclosed mature adipocytes proliferate in vitro. Both mRNA and protein expression analyses for hypoxia regulated genes, such as vascular endothelial growth factor (VEGF) and heme oxygenase 1 (HO1), showed that mature adipocytes of wild type mice respond to hypoxia. In contrast, mature adipocytes of diabetic db/db and TallyHo mice did not efficiently respond to hypoxia. Our studies suggest that mature adipocytes are functionally active cells, and their abnormal function to hypoxia can be one of underlining mechanisms in type 2 d...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5058049</comments>
            <pubDate>Wed, 13 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5058049</guid>        </item>
        <item>
            <title>A new long term in vitro model of myelination.</title>
            <link>http://www.medworm.com/index.php?rid=5058048&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21777582%26dopt%3DAbstract</link>
            <description>We describe (in terms of protein expression kinetic) a new in vitro model of sensory neurons/SC co-cultures presenting the following advantages: both sensory neurons and SC originate from the same individual; sensory neurons and SC being dissociated, they can be co-cultured in monolayer, allowing an easier microscope observation; the co-culture can be maintained in a serum-free medium for at less three months, allowing kinetic studies of myelin formation both at a molecular and cellular level. Optimizing culture conditions permits to use 96-well culture plates; image analyses conducted with an automatic image analyzer allows rapid, accurate and quantitative expression of results. Finally, this system was proved by measuring the apparition of myelin protein to mimic in vitro the physiologic...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5058048</comments>
            <pubDate>Mon, 11 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5058048</guid>        </item>
        <item>
            <title>Downregulation of tight junction-associated MARVEL protein marvelD3 during epithelial-mesenchymal transition in human pancreatic cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5058051&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21763689%26dopt%3DAbstract</link>
            <description>In conclusion, marvelD3 is transcriptionally downregulated in Snail-induced EMT during the progression for the pancreatic cancer.
    PMID: 21763689 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5058051</comments>
            <pubDate>Thu, 07 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5058051</guid>        </item>
        <item>
            <title>Proper regulation of Cdc42 activity is required for tight actin concentration at the equator during cytokinesis in adherent mammalian Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5058053&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21763307%26dopt%3DAbstract</link>
            <description>Authors: Zhu X, Wang J, Moriguchi K, Liow LT, Ahmed S, Kaverina I, Murata-Hori M
    Cytokinesis in mammalian cells requires actin assembly at the equatorial region. Although functions of RhoA in this process have been well established, additional mechanisms are likely involved. We have examined if Cdc42 is involved in actin assembly during cytokinesis. Depletion of Cdc42 had no apparent effects on the duration of cytokinesis, while overexpression of constitutively active Cdc42 (CACdc42) caused cytokinesis failure in normal rat kidney epithelial cells. Cells depleted of Cdc42 displayed abnormal cell morphology and caused a failure of tight accumulation of actin and RhoA at the equator. In contrast, in cells overexpressing CACdc42, actin formed abnormal bundles and RhoA was largely eliminat...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5058053</comments>
            <pubDate>Wed, 06 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5058053</guid>        </item>
        <item>
            <title>Control of growth cone motility and neurite outgrowth by SPIN90.</title>
            <link>http://www.medworm.com/index.php?rid=5058052&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21763308%26dopt%3DAbstract</link>
            <description>Authors: Kim SM, Bae J, Cho IH, Choi KY, Park YJ, Ryu JH, Chun JS, Song WK
    SPIN90 is an F-actin binding protein thought to play important roles in regulating cytoskeletal dynamics. It is known that SPIN90 is expressed during the early stages of neuronal development, but details of its localization and function in growth cones have not been fully investigated. Our immunocytochemical data show that SPIN90 is enriched throughout growth cones and neuronal shafts in young hippocampal neurons. We also found that its localization correlates with and depends upon the presence of F-actin. Detailed observation of primary cultures of hippocampal neurons revealed that SPIN90 knockout reduces both growth cone areas and in the numbers of filopodia, as compared to wild-type neurons. In addition, tota...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5058052</comments>
            <pubDate>Wed, 06 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5058052</guid>        </item>
        <item>
            <title>Alexander disease causing mutations in the C-terminal domain of GFAP are deleterious both to assembly and network formation with the potential to both activate caspase 3 and decrease cell viability.</title>
            <link>http://www.medworm.com/index.php?rid=5058056&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21756903%26dopt%3DAbstract</link>
            <description>Authors: Chen YS, Lim SC, Chen MH, Quinlan RA, Perng MD
    Alexander disease is a primary genetic disorder of astrocyte caused by dominant mutations in the astrocyte-specific intermediate filament glial fibrillary acidic protein (GFAP). While most of the disease-causing mutations described to date have been found in the conserved α-helical rod domain, some mutations are found in the C-terminal non-α-helical tail domain. Here, we compare five different mutations (N386I, S393I, S398F, S398Y and D417M14X) located in the C-terminal domain of GFAP on filament assembly properties in vitro and in transiently transfected cultured cells. All the mutations disrupted in vitro filament assembly. The mutations also affected the solubility and promoted filament aggregation of GFAP in transiently tran...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5058056</comments>
            <pubDate>Fri, 01 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5058056</guid>        </item>
        <item>
            <title>KARP-1 works as a heterodimer with Ku70, but the function of KARP-1 cannot perfectly replace that of Ku80 in DSB repair.</title>
            <link>http://www.medworm.com/index.php?rid=5058055&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21756904%26dopt%3DAbstract</link>
            <description>In this study, we established and characterized EGFP-KARP-1-expressing xrs-6 cell lines, EGFP-KARP-1/xrs-6. We found that nuclear localization signal (NLS) of KARP-1 is localized in the C-terminal region. Our data showed that KARP-1 localizes within the nucleus in NLS-dependent and NLS-independent manner and forms a heterodimer with Ku70, and stabilizes Ku70. On the other hand, EGFP-KARP-1 could not perfectly complement the radiosensitivity and DSB repair activity of Ku80-deficient xrs-6 cells. Furthermore, KARP-1 could not accumulate at DSBs faster than Ku80, although EGFP-KARP-1 accumulates at DSBs. Our data demonstrate that the function of KARP-1 could not perfectly replace that of Ku80 in DSB repair, although KARP-1 has some biochemical properties, which resemble those of Ku80, and wor...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5058055</comments>
            <pubDate>Fri, 01 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5058055</guid>        </item>
        <item>
            <title>Downregulation of FLIP by cycloheximide sensitizes human fat cells to CD95-induced apoptosis.</title>
            <link>http://www.medworm.com/index.php?rid=5058054&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21756905%26dopt%3DAbstract</link>
            <description>In conclusion, we identify FLIP as an important regulator of apoptosis sensitivity in fat cells. Modulating adipocyte homeostasis by apoptosis might provide a new therapeutic concept to get rid of excess adipose tissue, and FLIP might be a possible target molecule.
    PMID: 21756905 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5058054</comments>
            <pubDate>Fri, 01 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5058054</guid>        </item>
        <item>
            <title>LAMMER kinase Kic1 is involved in pre-mRNA processing.</title>
            <link>http://www.medworm.com/index.php?rid=5058059&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21745468%26dopt%3DAbstract</link>
            <description>In this study, we demonstrate for the first time that Kic1 not only is required for efficient splicing but also affects mRNA export, providing evidence for the conserved roles of LAMMER kinases in the unicellular context of fission yeast. Consistent with the hypothesis of its direct participation in multiple steps of pre-mRNA processing, Kic1 is predominantly present in the nucleus during interphase. In addition, the kinase activity of Kic1 plays a role in modulating its own cellular partitioning. Interestingly, Kic1 expression oscillates in a cell cycle-dependent manner and the peak level coincides with mitosis and cytokinesis, revealing a potential mechanism for controlling the kinase activity during the cell cycle. The novel information about the in vivo functions and regulation of Kic1...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5058059</comments>
            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5058059</guid>        </item>
        <item>
            <title>Interleukin-4 enhances trafficking and functional activities of GM-CSF-stimulated mouse myeloid-derived dendritic cells at late differentiation stage.</title>
            <link>http://www.medworm.com/index.php?rid=5058060&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21741972%26dopt%3DAbstract</link>
            <description>In this study, we demonstrate that IL-4, a key driving factor for in vitro propagation and differentiation of BMDCs, when added during a late culture stage can enhance the in vivo trafficking activity of granulocyte-macrophage colony-stimulating factor (GM-CSF)-induced BMDCs. It suggests that the temporal control of IL-4 stimulation during the in vitro generation of DCs drastically affects the DC trafficking efficiency in vivo. With this modification of IL-4 stimulation, we also show that much less cytokine was needed to generate BMDCs with high purity and yield that secrete a high level of cytokines and possess a good capacity to induce proliferation of allogeneic CD4(+)T cells, as compared to the conventional method that uses a continuous supplement of GM-CSF and IL-4 throughout cultivat...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5058060</comments>
            <pubDate>Wed, 29 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5058060</guid>        </item>
        <item>
            <title>Notch signaling in intestinal homeostasis across species: the cases of Drosophila, Zebrafish and the mouse.</title>
            <link>http://www.medworm.com/index.php?rid=5058058&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21745469%26dopt%3DAbstract</link>
            <description>Authors: Fre S, Bardin A, Robine S, Louvard D
    Notch signaling has been recently shown to have a fundamental role in stem cell maintenance and control of proper homeostasis in the intestine of different species. Here, we briefly review the current literature on Notch signals in the intestine of Drosophila, Zebrafish and the mouse, and try to highlight conserved and divergent Notch functions across species. Notch signals show a remarkably conserved role in skewing cell fate choices in intestinal lineages throughout evolution. Genetic analysis demonstrates that loss of Notch signaling invariably leads to increased numbers of secretory cells and loss of enterocytes, while gain of Notch function will completely block secretory cell differentiation. Finally, we discuss the potential contribu...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5058058</comments>
            <pubDate>Wed, 29 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5058058</guid>        </item>
        <item>
            <title>Targeting the erythropoietin receptor on glioma cells reduces tumour growth.</title>
            <link>http://www.medworm.com/index.php?rid=5058057&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21749867%26dopt%3DAbstract</link>
            <description>Authors: Pérès E, Valable S, Guillamo JS, Marteau L, Bernaudin JF, Roussel S, Lechapt-Zalcman E, Bernaudin M, Petit E
    Hypoxia has been shown to be one of the major events involved in EPO expression. Accordingly, EPO might be expressed by cerebral neoplastic cells, especially in glioblastoma, known to be highly hypoxic tumours. The expression of EPOR has been described in glioma cells. However, data from the literature remain descriptive and controversial. On the basis of an endogenous source of EPO in the brain, we have focused on a potential role of EPOR in brain tumour growth. In the present study, with complementary approaches to target EPO/EPOR signalling, we demonstrate the presence of a functional EPO/EPOR system on glioma cells leading to the activation of the ERK pathway. Thi...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5058057</comments>
            <pubDate>Wed, 29 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5058057</guid>        </item>
        <item>
            <title>A new assay for functional screening of BRCA2 linker region mutations identifies variants that alter chemoresistance to cisplatin.</title>
            <link>http://www.medworm.com/index.php?rid=5058061&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21741379%26dopt%3DAbstract</link>
            <description>This study focused on the poorly studied linker region of the cancer-associated BRCA2 protein encoded by exons twelve through fourteen of BRCA2. To develop a new method to characterize VUS in this region of BRCA2, we first chose to study 4 reported VUS occurring on evolutionarily conserved residues within the linker region. To determine if these VUS represent neutral changes or if they impact the function of the BRCA2 protein, we stably transfected expression plasmids encoding wild-type or each mutant peptide into T47D breast cancer cells, which are wild-type for BRCA2. Four mutant peptide expressing cell lines and a wild-type linker region expressing cell line next were studied by challenging transfected cell lines with the DNA crosslinking compound cisplatin (10μM) for 5days. Expression...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5058061</comments>
            <pubDate>Tue, 28 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5058061</guid>        </item>
        <item>
            <title>Tenascin-C in the extracellular matrix promotes the selection of highly proliferative and tubulogenesis-defective endothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=5058062&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21740900%26dopt%3DAbstract</link>
            <description>Authors: Alves TR, da Fonseca AC, Nunes SS, da Silva AO, Dubois LG, Faria J, Kahn SA, Viana NB, Marcondes J, Legrand C, Moura-Neto V, Morandi V
    The extracellular matrix (ECM) contains important cues for tissue homeostasis and morphogenesis. The matricellular protein tenascin-C (TN-C) is overexpressed in remodeling tissues and cancer. In the present work, we studied the effect of different ECM-which exhibited a significant diversity in their TN-C content-in endothelial survival, proliferation and tubulogenic differentiation: autologous (endothelial) ECM devoid of TN-C, but bearing large amounts of FN; fibroblast ECM, bearing both high TN-C and FN contents; and finally, glioma-derived matrices, usually poor in FN, but very rich in TN-C. HUVECs initially adhered to the immobilized matrix ...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5058062</comments>
            <pubDate>Fri, 24 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5058062</guid>        </item>
        <item>
            <title>Inhibition of glycogen synthase kinase-3 enhances the differentiation and reduces the proliferation of adult human olfactory epithelium neural precursors.</title>
            <link>http://www.medworm.com/index.php?rid=5009167&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21708147%26dopt%3DAbstract</link>
            <description>In this study, we examined the impact of decreased GSK-3 activity on the fate of adult human OE neural precursors in vitro. GSK-3 inhibition was achieved using ATP-competitive (6-bromoindirubin-3'-oxime and CHIR99021) or substrate-competitive (TAT-eIF2B) inhibitors to eliminate potential confounding effects on cell fate due to off-target kinase inhibition. GSK-3 inhibitors decreased the number of neural precursor cells in OE cell cultures through a reduction in proliferation. Decreased proliferation was not associated with a reduction in cell survival but was accompanied by a reduction in nestin expression and a substantial increase in the expression of the neuronal differentiation markers MAP1B and neurofilament (NF-M) after 10days in culture. Taken together, these results suggest that GS...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5009167</comments>
            <pubDate>Fri, 24 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5009167</guid>        </item>
        <item>
            <title>A C-terminal PDZ binding domain modulates the function and localization of Kv1.3 channels.</title>
            <link>http://www.medworm.com/index.php?rid=5009163&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21726550%26dopt%3DAbstract</link>
            <description>Authors: Doczi MA, Damon DH, Morielli AD
    The voltage-gated potassium channel, Kv1.3, plays an important role in regulating membrane excitability in diverse cell types ranging from T-lymphocytes to neurons. In the present study, we test the hypothesis that the C-terminal PDZ binding domain modulates the function and localization of Kv1.3. We created a mutant form of Kv1.3 that lacked the last three amino acids of the C-terminal PDZ-binding domain (Kv1.3ΔTDV). This form of Kv1.3 did not bind the PDZ domain containing protein, PSD95. We transfected wild type and mutant Kv1.3 into HEK293 cells and determined if the mutation affected current, Golgi localization, and surface expression of the channel. We found that cells transfected with Kv1.3ΔTDV had greater current and lower Golgi locali...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5009163</comments>
            <pubDate>Fri, 24 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5009163</guid>        </item>
        <item>
            <title>Angiopoietins-1 and -2 play opposing roles in endothelial sprouting of embryoid bodies in 3D culture and their receptor Tie-2 associates with the cell-cell adhesion molecule PECAM1.</title>
            <link>http://www.medworm.com/index.php?rid=5009165&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21723278%26dopt%3DAbstract</link>
            <description>Authors: Gu A, Shively JE
    Angiopoietins 1 and 2, ligands for the receptor kinase Tie-2, have been proposed to play critical but opposing roles in vascular development. Since signaling by Tie-2 is likely affected by other endothelial cell receptors such as Flk-1, the receptor for VEGF, and cell-cell adhesion receptors PECAM1 and VE-cad, we explored their interactions in a 3D model of vasculogenesis. When murine embryoid bodies (EBs) were treated with VEGF in Matrigel in the presence or absence of Ang-1 or Ang-2 for eight days, Ang-1 abrogated vascular sprouting for treatments started at days 0 or 3. In contrast, Ang-2 greatly accelerated vascular sprouting compared to untreated EBs. These results were confirmed in a second model system where VEGF treated HUVECs were grown in Matrigel in...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5009165</comments>
            <pubDate>Wed, 22 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5009165</guid>        </item>
        <item>
            <title>BAG-1L promotes keratinocyte differentiation in organotypic culture models and changes in relative BAG-1 isoform abundance may lead to defective stratification.</title>
            <link>http://www.medworm.com/index.php?rid=5009164&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21723279%26dopt%3DAbstract</link>
            <description>In this study we questioned whether BAG-1L or the shorter isoforms would promote keratinocyte differentiation in organotypic cultures of HaCaT. HaCaT parental and vector cells showed stratification, but terminal differentiation was not complete. Cultures overexpressing BAG-1L isoform-specifically were of increased thickness, demonstrated pronounced expression of basal cytokeratin 5 and β1-integrin, suprabasal involucrin, cytokeratin 1 and plasma membrane-localised filaggrin, and a marked keratinized layer of cells at the surface. We were unable to overexpress BAG-1S and BAG-1M isoform-specifically. Overexpression of BAG-1M gave rise to organotypic cultures intermediate in differentiation to controls and those overexpressing BAG-1L. Cells overexpressing BAG-1S also exhibited elevated endog...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5009164</comments>
            <pubDate>Wed, 22 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5009164</guid>        </item>
        <item>
            <title>Mislocalization of large ARF-GEFs as a potential mechanism for BFA resistance in COG-deficient cells.</title>
            <link>http://www.medworm.com/index.php?rid=5009166&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21722633%26dopt%3DAbstract</link>
            <description>Authors: Flanagan-Steet H, Johnson S, Smith RD, Bangiyeva J, Lupashin V, Steet R
    Defects in subunits of the conserved oligomeric Golgi (COG) complex represent a growing subset of congenital disorders of glycosylation (CDGs). In addition to altered protein glycosylation and vesicular trafficking, Cog-deficient patient fibroblasts exhibit a striking delay in the Golgi-disrupting effects of brefeldin A (BFA). Despite the diagnostic value of this BFA resistance, the molecular basis of this response is not known. To investigate potential mechanisms of resistance, we analyzed the localization of the large ARF-GEF, GBF1, in several Cog-deficient cell lines. Our results revealed mislocalization of GBF1 to non-Golgi compartments, in particular the ERGIC, within these cells. Biochemical analysis...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5009166</comments>
            <pubDate>Tue, 21 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5009166</guid>        </item>
        <item>
            <title>Bone morphogenetic protein -4 and -5 in pancreatic cancer-Novel bidirectional players.</title>
            <link>http://www.medworm.com/index.php?rid=5009169&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21704030%26dopt%3DAbstract</link>
            <description>Authors: Virtanen S, Alarmo EL, Sandström S, Ampuja M, Kallioniemi A
    Bone morphogenetic proteins (BMPs) are multifunctional signaling molecules that have gained increasing interest in cancer research. To obtain a systematic view on BMP signaling in pancreatic cancer we first determined the mRNA expression levels of seven BMP ligands (BMP2-BMP8) and six BMP specific receptors in pancreatic cancer cell lines and normal pancreatic tissue. BMP receptor expression was seen in all cancer and normal samples. Low expression levels of BMP5 and BMP8 were detected in cancer cells compared to the normal samples, whereas BMP4 expression was elevated in 25% of the cases. The impact of BMP4 and BMP5 signaling on cell phenotype was then evaluated in five pancreatic cancer cell lines. Both ligands sup...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5009169</comments>
            <pubDate>Thu, 16 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5009169</guid>        </item>
        <item>
            <title>Indispensable role of factor for adipocyte differentiation 104 (fad104) in lung maturation.</title>
            <link>http://www.medworm.com/index.php?rid=5009168&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21704616%26dopt%3DAbstract</link>
            <description>Authors: Kishimoto K, Nishizuka M, Ueda T, Kajita K, Ugawa S, Shimada S, Osada S, Imagawa M
    Factor for adipocyte differentiation 104 (fad104) is a regulator of adipogenesis and osteogenesis. Our previous study showed that fad104-deficient mice died immediately after birth, suggesting fad104 to be essential for neonatal survival. However, the cause of this rapid death is unclear. Here, we demonstrate the role of fad104 in neonatal survival. Phenotypic and morphological analyses showed that fad104-deficient mice died due to cyanosis-associated lung dysplasia including atelectasis. Furthermore, immunohistochemistry revealed that FAD104 was strongly expressed in ATII cells in the developing lung. Most importantly, the ATII cells in lungs were immature, and impaired the expression of surfac...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5009168</comments>
            <pubDate>Thu, 16 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5009168</guid>        </item>
        <item>
            <title>Mouse thymic epithelial cell lines expressing &quot;Aire&quot; and peripheral tissue-specific antigens reproduce in vitro negative selection of T cells.</title>
            <link>http://www.medworm.com/index.php?rid=4961722&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21683072%26dopt%3DAbstract</link>
            <description>Mouse thymic epithelial cell lines expressing &quot;Aire&quot; and peripheral tissue-specific antigens reproduce in vitro negative selection of T cells.
    Exp Cell Res. 2011 Jun 15;
    Authors: Yamaguchi Y, Takayanagi A, Chen J, Sakai K, Kudoh J, Shimizu N
    In the human thymus, AIRE (autoimmune regulator) gene is expressed in a very limited type of medullary thymic epithelial cells (mTECs) and no cognate cell lines are available, hence the molecular analysis of AIRE gene function has been difficult. To improve this situation, we attempted to isolate Aire-expressing cells and established three cell lines (Aire(+)TEC1, Aire(+)TEC2, Aire(+)DC) from the abnormally enlarged thymus, which was developed in the transgenic mice expressing SV40 T-antigen driven by the mouse Aire gene promoter. When thes...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961722</comments>
            <pubDate>Tue, 14 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4961722</guid>        </item>
        <item>
            <title>IGF2 derived from SH-SY5Y neuroblastoma cells induces the osteoclastogenesis of human monocytic precursors.</title>
            <link>http://www.medworm.com/index.php?rid=4961726&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21672538%26dopt%3DAbstract</link>
            <description>Authors: Avnet S, Salerno M, Quacquaruccio G, Granchi D, Giunti A, Baldini N
    The insulin-like growth factors 2 (IGF2) is a peptide hormone that binds to the insulin-like growth factor 1 receptor (IGF1R) and is abundantly stored in bone. IGF1R is deeply involved in the pathogenesis of many cancers that growth within bone and is also involved in osteoclast biology. Among different cell lines representative of osteolytic tumors, we found a very high expression of IGF2 in SH-SY5Y cells derived from neuroblastoma (NB). We previously showed that NB cells induce an osteolytic process through the Osteoprotegerin/RANKL/RANK and the canonical Wnt pathway system. Here, we hypothesized that NB promotes osteoclastogenesis also via IGF2. First, we demonstrated the presence of IGF1R on the osteoclast...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961726</comments>
            <pubDate>Fri, 10 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4961726</guid>        </item>
        <item>
            <title>Identification and characterization of protein interactions in the mammalian mRNA processing body using a novel two-hybrid assay.</title>
            <link>http://www.medworm.com/index.php?rid=4961725&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21672539%26dopt%3DAbstract</link>
            <description>Authors: Bloch DB, Nobre RA, Bernstein GA, Yang WH
    Components of the mRNA processing body (P-body) regulate critical steps in mRNA storage, transport, translation and degradation. At the core of the P-body is the decapping complex, which removes the 5' cap from de-adenylated mRNAs and mediates an irreversible step in mRNA degradation. The assembly of P-bodies in Saccharomyces cerevisiae, Arabidopsis thaliana and Drosophila melanogaster has been previously described. Less is known about the assembly of mammalian P-bodies. To investigate the interactions that occur between components of mammalian P-bodies, we developed a fluorescence-based, two-hybrid assay system. The assay depends on the ability of one P-body component, fused to an exogenous nuclear localization sequence (NLS), to recr...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961725</comments>
            <pubDate>Mon, 06 Jun 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>P43-dependent mitochondrial activity regulates myoblast differentiation and slow myosin isoform expression by control of Calcineurin expression.</title>
            <link>http://www.medworm.com/index.php?rid=4961731&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21664352%26dopt%3DAbstract</link>
            <description>In conclusion, these data clearly suggest that, partly via Calcineurin expression, mitochondrial protein synthesis is involved in muscle development through the control of myoblast differentiation and probably the acquisition of the contractile and metabolic phenotype of muscle fibres.
    PMID: 21664352 [PubMed - as supplied by publisher] (Source: Experimental Cell Research)</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961731</comments>
            <pubDate>Sun, 05 Jun 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Cell type-specific transcriptional regulation of the gene encoding importin-α1.</title>
            <link>http://www.medworm.com/index.php?rid=4961729&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21664354%26dopt%3DAbstract</link>
            <description>In this study, we identified a critical promoter region in Kpna2 and showed that the expression of this gene is differentially regulated in ES cells and NIH3T3 cells. Conserved CCAAT boxes are required for Kpna2 promoter activity in both ES and NIH3T3 cells. Interestingly, deletion of the region from nucleotide position -251 to -179bp resulted in a drastic reduction in Kpna2 transcriptional activity only in ES cells. This region contains Krüppel-like factor (Klf) binding sequences and is responsible for transactivation of the gene by Klf2 and Klf4. Accordingly, endogenous Kpna2 mRNA levels decreased in response to depletion of Klf2 and Klf4 in ES cells. Our results suggest that Klf2 and Klf4 function redundantly to drive high level of Kpna2 expression in ES cells.
    PMID: 21664354 [PubM...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961729</comments>
            <pubDate>Sun, 05 Jun 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>NHE1 mediates MDA-MB-231 cells invasion through the regulation of MT1-MMP.</title>
            <link>http://www.medworm.com/index.php?rid=4961728&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21669197%26dopt%3DAbstract</link>
            <description>Authors: Lin Y, Chang G, Wang J, Jin W, Wang L, Li H, Ma L, Li Q, Pang T
    Na(+)/H(+) exchanger 1 (NHE1), an important regulator of intracellular pH (pH(i)) and extracellular pH (pH(e)), has been shown to play a key role in breast cancer metastasis. However, the exact mechanism by which NHE1 mediates breast cancer metastasis is not yet well known. We showed here that inhibition of NHE1 activity, with specific inhibitor Cariporide, could suppress MDA-MB-231 cells invasion as well as the activity and expression of MT1-MMP. Overexpression of MT1-MMP resulted in a distinguished increase in MDA-MB-231 cells invasiveness, but treatment with Cariporide reversed the MT1-MMP-mediated enhanced invasiveness. To explore the role of MAPK signaling pathways in NHE1-mediated breast cancer metastasis, w...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4961728</comments>
            <pubDate>Sun, 05 Jun 2011 23:00:00 +0100</pubDate>
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            <title>OSBP-related protein 7 interacts with GATE-16 and negatively regulates GS28 protein stability.</title>
            <link>http://www.medworm.com/index.php?rid=4961727&amp;cid=s_35561_171_f&amp;fid=35561&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21669198%26dopt%3DAbstract</link>
            <description>In this study, we identified by yeast two-hybrid screening an interaction partner of ORP7, GATE-16, which (i) regulates Golgi SNARE of 28kDa (GS28) function and stability, and (ii) plays a role in autophagosome biogenesis. The interaction was confirmed by bimolecular fluorescence complementation (BiFC) assay in living cells. The interacting regions were delineated within aa 1-142 of ORP7 and aa 30-117 of GATE-16. ORP7 knock-down in 293A cells resulted in a 40% increase of GS28 protein while ORP7 overexpression had the opposite effect (25% decrease of GS28). We show evidence that the regulation of GS28 by ORP7 does not occur at the level of transcription, but involves degradation of GS28 on proteasomes. Truncated ORP7 that lacks the GATE-16 binding region failed to affect GS28 stability, ev...</description>
            <author>Experimental Cell Research</author>
            <type>journals</type>
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            <pubDate>Sun, 05 Jun 2011 23:00:00 +0100</pubDate>
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