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 'Cell Cycle' source. Tue, 07 Feb 2012 08:48:52 +0100 http://www.medworm.com/index.php?rid=5659097&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22293493%26dopt%3DAbstract Authors: Basu A, Banerjee P, Pal S Abstract Comment on: Basu A, et al. PLoS One 2011; 6:e23919. PMID: 22293493 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5659097 Sun, 05 Feb 2012 07:06:27 +0100 5659097 http://www.medworm.com/index.php?rid=5659096&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22293494%26dopt%3DAbstract In conclusion, our studies show p53 as a determining factor for induction of apoptosis vs. polyploidy upon inhibition of Aurora A. PMID: 22293494 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5659096 Sun, 05 Feb 2012 07:06:17 +0100 5659096 http://www.medworm.com/index.php?rid=5659100&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22293402%26dopt%3DAbstract Authors: Ramsay R Abstract Comment on: Cesi V, et al. Cell Cycle 2011; 10:4149-61. PMID: 22293402 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5659100 Wed, 01 Feb 2012 05:00:00 +0100 5659100 http://www.medworm.com/index.php?rid=5659099&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22293403%26dopt%3DAbstract Authors: Landes RG PMID: 22293403 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5659099 Wed, 01 Feb 2012 05:00:00 +0100 5659099 http://www.medworm.com/index.php?rid=5659098&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22293404%26dopt%3DAbstract Authors: Icreverzi A, de la Cruz A, Van Voorhies W, Edgar B Abstract Drosophila cyclinD (CycD) is the single fly ortholog of the mammalian cyclin D1 and promotes both cell cycle progression and cellular growth. However, little is known about how CycD promotes cell growth. We show here that CycD/Cdk4 hyperactivity leads to increased mitochondrial biogenesis (mitobiogenesis), mitochondrial mass, NRF-1 activity (Tfam transcript levels) and metabolic activity in Drosophila, whereas loss of CycD/Cdk4 activity has the opposite effects. Surprisingly, both CycD/Cdk4 addition and loss of function increase mitochondrial superoxide production and decrease lifespan, indicating that an imbalance in mitobiogenesis may lead to oxidative stress and aging. In addition, we provide multiple lines of ... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5659098 Wed, 01 Feb 2012 05:00:00 +0100 5659098 http://www.medworm.com/index.php?rid=5640053&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22274398%26dopt%3DAbstract In this study, we demonstrated that the Salmonella typhimurium A1-R tumor-targeting strain can inhibit and eradicate human glioma in an orthotopic nude-mouse model. S. typhimurium A1-R was administered by injection through a craniotomy open-window or intravenously in nude mice. To establish the model, 2 x 105 U87-RFP human glioma cells were injected stereotactically into the mouse brain through the craniotomy open window. Two weeks after glioma-cell implantation, mice were treated with S. typhimurium A1-R [2 x 10 ( 7) CFU/200 μl intravenous injection (i.v.) or 1 x 10 ( 6) CFU/1 μl intracranial injection (i.c.)] once a week for 3 weeks. Brain tumors were observed by fluorescence imaging through the craniotomy open window over time. S. typhimurium A1-R, administered i.c., inhibited brain t... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5640053 Mon, 30 Jan 2012 08:36:30 +0100 5640053 http://www.medworm.com/index.php?rid=5640052&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22274399%26dopt%3DAbstract Authors: Lehman NL, O'Donnell JP, Whiteley LJ, Stapp RT, Lehman TD, Roszka KM, Schultz LR, Williams CJ, Mikkelsen T, Brown SL, Ecsedy JA, Poisson LM Abstract Aurora A is critical for mitosis and is overexpressed in several neoplasms. Its overexpression transforms cultured cells, and both its overexpression and knockdown cause genomic instability. In transgenic mice, Aurora A haploinsufficiency, not overexpression, leads to increased malignant tumor formation. Aurora A thus appears to have both tumor-promoting and tumor-suppressor functions. Here, we report that Aurora A protein, measured by quantitative protein gel blotting, is differentially expressed in major glioma types in lineage-specific patterns. Aurora A protein levels in WHO grade II oligodendrogliomas (n = 16) and grade I... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5640052 Mon, 30 Jan 2012 08:36:21 +0100 5640052 http://www.medworm.com/index.php?rid=5640050&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22274400%26dopt%3DAbstract In this report, we extend our recent studies and further the notion that the stoichiometric balance between RIP1 and cIAPs is critical for Ripoptosome formation. Furthermore, we demonstrate the critical relevance of the balance of expression levels of short (cFLIPS) or viral (vFLIP) forms of FLIP and RIP3 kinase for the spontaneous execution of necroptosis whenever cIAPs are absent in the cells. Our study thus supports and extends the intriguing role of the Ripoptosome for the regulation of apoptosis and necroptosis. PMID: 22274400 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5640050 Mon, 30 Jan 2012 08:36:11 +0100 5640050 http://www.medworm.com/index.php?rid=5623120&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262166%26dopt%3DAbstract In this study, we tested mTorKIs against a large panel of colorectal cancer (CRC) cell lines, and found that mTorKIs displayed broader anti-CRC activity than rapamycin, including CRC cells with K-Ras or B-Raf mutations, suggesting that these mTorKIs are particularly useful for CRCs resistant to EGFR inhibitors. Unexpectedly, we found that 40% CRC cell lines were intrinsically drug resistant. Moreover, we discovered an mTO R-independent 4E‑ BP1 phosphorylation that was correlated with mTorKI resistance. Altogether, our findings provide compelling preclinical support for testing mTorKIs in human CRC clinical trials. They further reveal the existence of significant intrinsic mTorKI drug resistance in cancer cells and suggest that 4E-BP1 phosphorylation is a predictive biomarker for mTorKI s... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623120 Tue, 24 Jan 2012 09:53:01 +0100 5623120 http://www.medworm.com/index.php?rid=5623119&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262167%26dopt%3DAbstract Authors: Yang H, Zheng Z, Zhao L, Li Q, Liao D Abstract Successful viral replication entails elimination or bypass of host antiviral mechanisms. Here, we show that shRNA-mediated knockdown of murine double minute (Mdm2) and its paralog Mdm4 enhanced the expression of early and late viral gene products during adenovirus (HAdV) infection. Remarkably, whereas the expression of HAdV genes was low in p53-deficient mouse embryonic fibroblasts (p53KO MEFs), the HAdV early gene products were efficiently expressed in Mdm2/p53 double-knockout (DKO) and Mdm4/p53 DKO MEFs, and viral capsid proteins were produced in Mdm2/p53 DKO MEFs. Thus, Mdm2 and Mdm4 seem to have potent antiviral property. In cells infected with wt HAdV or a mutant virus lacking the E1B-55K gene (dl 1520), both Mdm2 and Mdm... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623119 Tue, 24 Jan 2012 09:52:50 +0100 5623119 http://www.medworm.com/index.php?rid=5623118&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262168%26dopt%3DAbstract We report here the generation and characterization of SGO1-mutant mice and show that haploinsufficiency of SGO1 leads to enhanced colonic tumorigenesis. Complete disruption of SGO1 results in embryonic lethality, whereas SGO1 (+/-) mice are viable and fertile. Haploinsufficiency of SGO1 results in genomic instability manifested as missegregation of chromosomes and formation of extra centrosomal foci in both murine embryonic fibroblasts and adult bone marrow cells. Enhanced CIN observed in SGO1-deficient mice resulted in an increase in formation of aberrant crypt foci (ACF) and accelerated development of tumors after exposure to azoxymethane (AOM), a colon carcinogen. Together, these results suggest that haploinsufficiency of SGO1 causes enhanced CIN, colonic preneoplastic lesions and tumor... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623118 Tue, 24 Jan 2012 09:52:38 +0100 5623118 http://www.medworm.com/index.php?rid=5623117&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262169%26dopt%3DAbstract Authors: Walter G, Ruediger R Abstract Evidence that protein phosphatase 2A (PP2A) is a tumor suppressor in humans came from the discovery of mutations in the genes encoding the Aα and Aβ subunits of the PP2A trimeric holoenzymes, Aα-B-C and Aβ-B-C. One point mutation, Aα-E64D, was found in a human lung carcinoma. It renders Aα specifically defective in binding regulatory B' subunits. Recently, we reported a knock-in mouse expressing Aα-E64D and an Aα knockout mouse. The mutant mice showed a 50-60% increase in the incidence of lung cancer induced by benzopyrene. Importantly, PP2A's tumor suppressor activity depended on p53. These data provide the first direct evidence that PP2A is a tumor suppressor in mice. In addition, they suggest that PP2A is a tumor suppressor in human... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623117 Tue, 24 Jan 2012 09:52:27 +0100 5623117 http://www.medworm.com/index.php?rid=5623116&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262170%26dopt%3DAbstract Authors: Veldhoen M PMID: 22262170 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623116 Tue, 24 Jan 2012 09:52:16 +0100 5623116 http://www.medworm.com/index.php?rid=5623115&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262171%26dopt%3DAbstract In this study, we demonstrate that there is no obvious different cytotoxic response between cancer cells with and without functional p53, including the isogenic colon cancer cell lines HCT116p53(+/+) and HCT116p53(-/-), breast cancer cell line MCF7, lung cancer cell line A549 and cervical carcinoma cell line HeLa, after treatment with either siRNA against Plk1, the kinase domain inhibitors BI 2536 and BI 6727 or the PBD inhibitor Poloxin. We suggest that the p53 status is not a predictor for the response of Plk1 inhibition, at least not directly. Yet, the long-term outcomes of losing p53, such as genome instability, could be associated with the cytotoxicity of Plk1 inhibition. Further studies are required to investigate whether other circumstances of cancer cells, such as DNA replication/d... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623115 Tue, 24 Jan 2012 09:52:05 +0100 5623115 http://www.medworm.com/index.php?rid=5623094&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262172%26dopt%3DAbstract Authors: Rosner M, Schipany K, Hengstschläger M Abstract Comment on: Rosner M, et al. Amino Acids 2011; In press. PMID: 22262172 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623094 Tue, 24 Jan 2012 09:51:53 +0100 5623094 http://www.medworm.com/index.php?rid=5623093&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262173%26dopt%3DAbstract Authors: Pöling J, Gajawada P, Lörchner H, Polyakowa V, Szibor M, Böttger T, Warnecke H, Kubin T, Braun T Abstract Dedifferentiation is a common phenomenon among plants but has only been found rarely in vertebrates where it is mostly associated with regenerative responses such as formation of blastemae in amphibians to initiate replacement of lost body parts. Relatively little attention has been paid to dedifferentiation processes in mammals although a decline of differentiated functions and acquisition of immature, "embryonic" properties is seen in various disease processes. Dedifferentiation of parenchymal cells in mammals might serve multiple purposes including (1) facilitation of tissue regeneration by generation of progenitor-like cells and (2) protection of cells from hypo... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623093 Tue, 24 Jan 2012 09:51:42 +0100 5623093 http://www.medworm.com/index.php?rid=5623092&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262174%26dopt%3DAbstract Authors: Narasimhachar Y, Webster DR, Gard DL, Coué M Abstract During the maturation of Xenopus oocytes, Cdc6 expression is necessary to establish replication competence to support early embryonic DNA replication. However, Cdc6 is expressed before the completion of MI, at a time when its function as a replication factor is not required, suggesting additional roles for Cdc6 in meiosis. Confocal immunofluorescence microscopy revealed that Cdc6 protein was distributed around the spindle precursor at the time of germinal vesicle breakdown (GVBD), and localized to the margin of the nascent spindle early in prometaphase. Cdc6 subsequently localized to spindle poles in late prometaphase, where it remained until metaphase arrest. Microinjection of antisense oligonucleotides specific for C... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623092 Tue, 24 Jan 2012 09:51:30 +0100 5623092 http://www.medworm.com/index.php?rid=5623085&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262175%26dopt%3DAbstract Authors: Naito Y, Shimizu H, Kasama T, Sato J, Tabara H, Okamoto A, Yabuta N, Nojima H Abstract Protein phosphatase 2A (PP 2A) bearing the B'γ (= B'α/B56γ1/PR61γ) subunit is recruited to dephosphorylation targets by cyclin G. We demonstrate here that cyclin G-associated kinase (GAK), a component of the GAK/B'γ/cyclin G complex, directly phosphorylates the B'γ-Thr104 residue and regulates PP 2A activity. Indeed, an anti-B'γ-pT104 antibody detected immunofluorescence signals at the chromosome and centrosome during mitosis; these signals were reduced by siRNAmediated GAK knockdown. After DNA damage by γ-irradiation, the chromosome signals formed foci that colocalized with a DNA double-strand break (DSB) marker H2AX-pS139 (γH2AX) and CHK2-pT68. Moreover, B'γ-pT104 enhanced PP... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623085 Tue, 24 Jan 2012 09:51:19 +0100 5623085 http://www.medworm.com/index.php?rid=5623084&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262176%26dopt%3DAbstract Authors: Morgado-Palacin L, Llanos S, Serrano M Abstract Ribosome biogenesis is the most demanding energetic process in proliferating cells and it is emerging as a critical sensor of cellular homeostasis. Upon disturbance of ribosome biogenesis, specific free ribosomal proteins, most notably L11, bind and inhibit Mdm2, resulting in activation of the tumor suppressor p53. This pathway has been characterized in somatic and cancer cells, but its function in embryonic pluripotent cells has remained unexplored. Here, we show that treatment with low doses of Actinomycin D or depletion of ribosomal protein L37, two well-established inducers of ribosomal stress, activate p53 in an L11-dependent manner in mouse embryonic stem cells (ESCs) and in induced pluripotent stem cells (iPSCs). Activ... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623084 Tue, 24 Jan 2012 09:51:07 +0100 5623084 http://www.medworm.com/index.php?rid=5623079&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262177%26dopt%3DAbstract Authors: Liguori L, Andolfo I, De Antonellis P, Aglio V, di Dato V, Marino N, Ivan Orlotti N, De Martino D, Capasso M, Petrosino G, Schramm A, Navas L, Paolo Tonini G, Eggert A, Iolascon A, Zollo M Abstract Through microarray analyses, we identified the Mpped2 gene as differentially expressed in two neuroblastoma cell lines induced to differentiation with all-trans retinoic acid. Mpped2 codes for a new metallophosphodiesterase protein, the expression of which inhibits cell proliferation and soft agar colony formation in SH -SY5Y cells. This inhibition is concomitant to an increased proportion of the cells in G0/G1 phase and enhanced caspase 3 activation, effects not seen for the other phosphodiesterases. A Mpped2-null mutation (H67R) abrogates these functions, which indicates that ... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623079 Tue, 24 Jan 2012 09:50:55 +0100 5623079 http://www.medworm.com/index.php?rid=5623078&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262178%26dopt%3DAbstract Authors: He H, Luo Y Abstract Integrated high-risk human papillomavirus (HPV) DNA was frequently detected in the genomes of cervical carcinoma cells. The HPV E6 and E7 oncoproteins disrupt the functions of tumor suppressors p53 and Rb; thus, understanding the mechanism by which HPV E6 and E7 gene expression is regulated in cancer cells is highly relevant to cancer biology. Brg1 is a catalytic subunit of the SWI/SNF chromatin remodeling complexes that function in the transcriptional regulation of certain cellular genes. Here, we show that knockdown of Brg1 in HeLa cells leads to cell cycle arrest, p53 and Rb protein accumulation and, interestingly, downregulated expression of HPV18 E6 and E7 genes. Brg1 binds the HPV18 LCR in a JunB- and p300-dependent manner and is required for eff... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623078 Tue, 24 Jan 2012 09:50:44 +0100 5623078 http://www.medworm.com/index.php?rid=5623077&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262179%26dopt%3DAbstract Authors: Ding Y, Sun X, Redfield M, Kushwaha S, Xu X Abstract Comment on: Ding Y, et al. Circ Res 2011; 109:658-69. PMID: 22262179 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623077 Tue, 24 Jan 2012 09:50:32 +0100 5623077 http://www.medworm.com/index.php?rid=5623076&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262180%26dopt%3DAbstract In this study, we showed that BCL2L12 and BCL2L12A were overexpressed in glioblastoma multiforme (GBM). Large-scale yeast two-hybrid screening showed that BCL2L12 was a GSK3b binding partner in a testis cDNA library. Our data demonstrated that GSK3b interacts with BCL2L12 but not BCL2L12A, whose C terminus lacks a binding region. We found that a BCL2L12 153-191 fragment located outside of the C-terminal BH2 motif is responsible for GSK3b binding. In contrast, no interaction was detected between BCL2L12A and GSK3b. In vitro kinase and l-phosphatase assays showed that GSK3b phosphorylates BCL2L12 at S156, while this site is absent on BCL2L12A. Moreover, our data also showed that the BCL2L12 153-191 fragment directly interrupted GSK3bmediated Tau phosphorylation in a dose-dependent manner. Ec... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623076 Tue, 24 Jan 2012 09:50:21 +0100 5623076 http://www.medworm.com/index.php?rid=5623075&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262181%26dopt%3DAbstract Authors: Cho KR Abstract Comment on: Wu R, et al. Clin Cancer Res 2011; 17:7359-72. PMID: 22262181 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623075 Tue, 24 Jan 2012 09:50:11 +0100 5623075 http://www.medworm.com/index.php?rid=5623073&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262182%26dopt%3DAbstract Authors: Chan TO, Pascal J, Armen R, Rodeck U Abstract AGC kinases, including the three Akt (protein kinase B) isoforms, protein kinase A (PKA) and all protein kinase C (PKC) isoforms, require activation loop phosphorylation (threonine 308 in Akt1) as well as phosphorylation of a C-terminal residue (serine 473 in Akt1) for catalytic activity and phosphorylation of downstream targets. Conversely, phosphatases reverse these phosphorylations. Virtually all cellular processes are affected by AGC kinases, a circumstance that has led to intense scrutiny of the molecular mechanisms that regulate phosphorylation of these kinases. Here, we review a new layer of control of phosphorylation in Akt, PKA and PKC pointing to ATP binding pocket occupancy as a means to decelerate dephosphorylation ... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623073 Tue, 24 Jan 2012 09:49:59 +0100 5623073 http://www.medworm.com/index.php?rid=5623072&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262183%26dopt%3DAbstract We described here that the human TRIM8 protein, a member of the TRIM family, is a new modulator of the p53-mediated tumor suppression mechanism. We showed that under stress conditions, such as UV exposure, p53 induced the expression of TRIM8, which in turn stabilized p53 leading to cell cycle arrest and reduction of cell proliferation through enhancement of CDKN1A (p21) and GADD45 expression. TRIM8 silencing reduced the capacity of p53 to activate genes involved in cell cycle arrest and DNA repair, in response to cellular stress. Concurrently, TRIM8 overexpression induced the degradation of the MDM2 protein, the principal regulator of p53 stability. Co-immunoprecipitation experiments showed that TRIM8 physically interacted with p53, impairing its interaction with MDM2. Altogether, our resu... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623072 Tue, 24 Jan 2012 09:49:48 +0100 5623072 http://www.medworm.com/index.php?rid=5623071&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262184%26dopt%3DAbstract Authors: Campbell H, Slatter T, Jeffs A, Mehta R, Rubio C, Baird M, Braithwaite A Abstract Autoimmune diseases are characterized by the immune system mounting a response against self. The exact etiology of autoimmune diseases and autoimmunity remain unclear. Here, we demonstrate that Δ133p53, an isoform of the tumor suppressor protein p53, is involved in the development of autoimmunity. We have previously generated a mouse model of Δ133p53 (Δ122p53). Δ122p53 mice develop an autoimmune/ inflammation-like phenotype that includes the production of autoantibodies, elevated levels of pro-inflammatory cytokines and lymphocyte aggregations in various organs. Microarray analysis reveals that expression of Δ122p53 induces a number of pro-inflammatory genes, including the STAT1 pathway ... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623071 Tue, 24 Jan 2012 09:49:36 +0100 5623071 http://www.medworm.com/index.php?rid=5623070&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262185%26dopt%3DAbstract Authors: Bowman TV, Trompouki E, Zon LI Abstract Comment on: Trompouki E, et al. Cell 2011; 147:577-89. PMID: 22262185 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623070 Tue, 24 Jan 2012 09:49:25 +0100 5623070 http://www.medworm.com/index.php?rid=5623069&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262186%26dopt%3DAbstract Authors: Botchkareva N Abstract Skin development, postnatal growth and regeneration are governed by complex and well-balanced programs of gene activation and silencing. The crosstalk between small non-coding microRNAs (miRNAs) and mRNAs is highly important for steadiness of signal transduction and transcriptional activities as well as for maintenance of homeostasis in many organs, including the skin. Recent data demonstrated that the expression of many genes, including cell type-specific master transcription regulators implicated in the control of skin development and homeostasis, is regulated by miRNAs. In addition, individual miRNAs could mediate the effects of these signaling pathways through being their downstream components. In turn, the expression of a major constituent of th... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623069 Tue, 24 Jan 2012 09:49:14 +0100 5623069 http://www.medworm.com/index.php?rid=5623068&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262187%26dopt%3DAbstract Authors: Atwood A, Kay SA Abstract Comment on: Atwood A, et al. Proc Natl Acad Sci U S A 2011; 108:18560-5. PMID: 22262187 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623068 Tue, 24 Jan 2012 09:49:02 +0100 5623068 http://www.medworm.com/index.php?rid=5623067&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262188%26dopt%3DAbstract Authors: Xu X Abstract Comment on: Hou P, et al. Cell Cycle 2012; 11:286-95. PMID: 22262188 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623067 Tue, 24 Jan 2012 09:48:50 +0100 5623067 http://www.medworm.com/index.php?rid=5623066&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262189%26dopt%3DAbstract Authors: Napoli M, Girardini JE, Del Sal G Abstract Comment on: Valenti F, et al. Cell Cycle 2011; 10:4330-40. PMID: 22262189 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623066 Tue, 24 Jan 2012 09:48:39 +0100 5623066 http://www.medworm.com/index.php?rid=5623065&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262190%26dopt%3DAbstract Authors: Johnson N, Shapiro GI Abstract Comment on: Nguyen D, et al. Cell Cycle 2011; 10:4074-82. PMID: 22262190 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623065 Tue, 24 Jan 2012 09:48:28 +0100 5623065 http://www.medworm.com/index.php?rid=5623060&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262191%26dopt%3DAbstract Authors: Cianfanelli V, Cecconi F Abstract Comment on: Criollo A, et al. Cell Cycle 2012; 11:194-9. PMID: 22262191 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623060 Tue, 24 Jan 2012 09:48:20 +0100 5623060 http://www.medworm.com/index.php?rid=5623059&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262192%26dopt%3DAbstract Authors: Ben-Aroya S Abstract Comment on: Levy-Barda A, et al. Cell Cycle 2011; 10:4300-10. PMID: 22262192 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623059 Tue, 24 Jan 2012 09:48:10 +0100 5623059 http://www.medworm.com/index.php?rid=5623122&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22234239%26dopt%3DAbstract Authors: Hysolli E, Tanaka Y, Kim KY, Jung YW, Park IH Abstract X-chromosome inactivation (XCI) is an important mechanism employed by mammalian XX female cells to level X-linked gene expression with that of male XY cells. XCI occurs early in development as the pluripotent cells of the inner cell mass (ICM) in blastocysts successively differentiate into cells of all three germ layers. X-chromosome reactivation (XCR), the reversal of XCI, is critical for germ cell formation as a mechanism to diversify the X-chromosome gene pool. Here we review the characterization of XCR, and further explore its natural occurrence during development and the in vitro models of cellular reprogramming. We also review the key regulators involved in XCI for their role in suppressing the active histone mar... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623122 Sun, 15 Jan 2012 05:00:00 +0100 5623122 http://www.medworm.com/index.php?rid=5623121&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22234241%26dopt%3DAbstract Authors: Ertel A, Tsirigos A, Whitaker-Menezes D, Birbe RC, Pavlides S, Martinez-Outschoorn UE, Pestell RG, Howell A, Sotgia F, Lisanti MP Abstract Aging drives large systemic reductions in oxidative mitochondrial function, shifting the entire body metabolically towards aerobic glycolysis, a.k.a, the Warburg effect. Aging is also one of the most significant risk factors for the development of human cancers, including breast tumors. How are these two findings connected? One simplistic idea is that cancer cells rebel against the aging process by increasing their capacity for oxidative mitochondrial metabolism (OXPHOS). Then, local and systemic aerobic glycolysis in the aging host would provide energy-rich mitochondrial fuels (such as L-lactate and ketones) to directly "fuel" tumor ce... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5623121 Sun, 15 Jan 2012 05:00:00 +0100 5623121 http://www.medworm.com/index.php?rid=5578509&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22214660%26dopt%3DAbstract Authors: Enserink JM, Kolodner RD Abstract Deregulated CDK activity drives cell proliferation of the majority of human tumors, making CDKs highly relevant research subjects. Cdc28 controls cell cycle progression in the budding yeast Saccharomyces cerevisiae, but the identity of many genes that function in conjunction with CDC28 to regulate the cell cycle and cell viability remains obscure. In a recent study, we used a chemical-genetic screen to identify the genetic network of CDC28. Through this analysis, we discovered that the Rad6-Bre1 pathway functions in this network and links ubiquitin levels to cell cycle progression by increasing transcription of cyclin genes. Thus, Rad6 boosts the activity of the cell cycle machinery. PMID: 22214660 [PubMed - as supplied by publisher] (... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5578509 Wed, 11 Jan 2012 16:03:06 +0100 5578509 http://www.medworm.com/index.php?rid=5578508&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22214661%26dopt%3DAbstract Authors: Weber JD, Gutmann DH Abstract In metazoans, TOR is an essential protein that functions as a master regulator of cellular growth and proliferation. Over the past decade, there has been an explosion of information about this critical master kinase, ranging from the composition of the TOR protein complex to its ability to act as an integrator of numerous extracellular signals. Unfortunately, this plethora of information has also raised numerous questions regarding TOR function. Currently, the prevailing view is that mammalian TOR (mTOR) exists in at least two molecular complexes, mTORC1 and mTORC2, which are largely defined by the presence of either RAPTOR or RICTOR. However, additional co-factors have been identified for each complex, and their importance in mediating mTOR s... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5578508 Wed, 11 Jan 2012 16:02:58 +0100 5578508 http://www.medworm.com/index.php?rid=5578507&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22214662%26dopt%3DAbstract Authors: Bennett R, Pan Y, Christian J, Hui T, May WS Abstract Cellular stresses, including growth factor deprivation, inflammatory cytokines or viral infection promote RAX/PACTdependent activation of the double-stranded RNA-dependent protein kinase, PKR, to phosphorylate eIF2α, resulting in translation inhibition and apoptosis. In addition, PKR has been reported to regulate p53, STAT1 and NFκB. Here, we report that RAX/PACT interacts with the SUMO E2 ligase Ubc9 to stimulate p53-Ubc9 association and reversible p53 sumoylation on lysine 386. In addition, expression of RAX/PACT in a variety of cell lines promotes p53 stability and activity to increase p53 target gene expression. Significantly, while the expression of RAX/PACT, PKR or p53 alone has little effect on the cell cycle o... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5578507 Wed, 11 Jan 2012 16:02:49 +0100 5578507 http://www.medworm.com/index.php?rid=5578506&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22214663%26dopt%3DAbstract Authors: Haupt S, Haupt Y Abstract Comment on: Valenti F, et al. Cell Cycle 2011; 10:4330-40. PMID: 22214663 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5578506 Wed, 11 Jan 2012 16:02:41 +0100 5578506 http://www.medworm.com/index.php?rid=5578505&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22214664%26dopt%3DAbstract Authors: Smrž D, Wilson TM, Metcalfe DD, Gilfillan AM Abstract Comment on: Smrž D, et al. Blood 2011; 118:6803-13. PMID: 22214664 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5578505 Wed, 11 Jan 2012 16:02:32 +0100 5578505 http://www.medworm.com/index.php?rid=5578504&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22214665%26dopt%3DAbstract Authors: Kaeberlein M, Kennedy BK PMID: 22214665 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5578504 Wed, 11 Jan 2012 16:02:23 +0100 5578504 http://www.medworm.com/index.php?rid=5578503&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22214666%26dopt%3DAbstract Authors: Rutkowski R, Gartner A Abstract Comment on: Lane DP, et al. Cell Cycle 2011; 10:4272-9. PMID: 22214666 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5578503 Wed, 11 Jan 2012 16:02:15 +0100 5578503 http://www.medworm.com/index.php?rid=5578502&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22214667%26dopt%3DAbstract Authors: Brabletz T Abstract Comment on: Siemens H, et al. Cell Cycle 2011; 10:4256-71. PMID: 22214667 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5578502 Wed, 11 Jan 2012 16:02:05 +0100 5578502 http://www.medworm.com/index.php?rid=5578501&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22214668%26dopt%3DAbstract Authors: Levine AJ Abstract Comment on: Lane DP, et al. Cell Cycle 2011; 10:4272-9. PMID: 22214668 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5578501 Wed, 11 Jan 2012 16:01:56 +0100 5578501 http://www.medworm.com/index.php?rid=5578500&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22214669%26dopt%3DAbstract Authors: Dumont J Abstract Comment on: Florian S, et al. Cell Cycle 2011; 10:3533-44. PMID: 22214669 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5578500 Wed, 11 Jan 2012 16:01:46 +0100 5578500 http://www.medworm.com/index.php?rid=5578499&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22214762%26dopt%3DAbstract Authors: Ritchey L, Ottman R, Roumanos M, Chakrabarti R Abstract Aurora kinase A (Aur-A), a mitotic kinase, regulates initiation of mitosis through centrosome separation and proper assembly of bipolar spindles. LIM kinase 1 (LIMK1), a modulator of actin and microtubule dynamics, is involved in the mitotic process through inactivating phosphorylation of cofilin. Phosphorylated LIMK1 is recruited to the centrosomes during early prophase, where it colocalizes with γ-tubulin. Here, we report a novel functional cooperativity between Aur-A and LIMK1 through mutual phosphorylation. LIMK1 is recruited to the centrosomes during early prophase and then to the spindle poles, where it colocalizes with Aur-A. Aur-A physically associates with LIMK1 and activates it through phosphorylation, whic... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5578499 Wed, 11 Jan 2012 16:01:35 +0100 5578499 http://www.medworm.com/index.php?rid=5578498&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22214763%26dopt%3DAbstract Authors: Schnerch D, Follo M, Krohs J, Felthaus J, Engelhardt M, Wäsch R Abstract Chromosome segregation is under strict control of the spindle assembly checkpoint (SAC). The SAC regulates anaphase-promoting complex/cyclosome (APC/C)-dependent proteolysis of securin and cyclin B. Unattached or misaligned chromosomes trigger SAC-mediated mitotic delay by stabilizing securin and cyclin B due to inhibition of APC/C until the problem is solved. Here we present a hitherto unavailable model facilitating the simultaneous depiction of chromosome movements and pulse-chased cyclin B proteolysis in every single cell within a cell population. During chromosome misalignment, we observed slow cyclin B degradation, which changed to fast degradation once the SAC was satisfied, initiating chromoso... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5578498 Wed, 11 Jan 2012 16:01:25 +0100 5578498 http://www.medworm.com/index.php?rid=5578497&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22214764%26dopt%3DAbstract In this study, we demonstrate that ZBP‑89 is essentially required in HDACi-mediated p21 upregulation in hepetocellular carcinoma (HCC). Overexpression of ZBP-89 protein enhanced the lethal effectiveness of Trichostatin A (TSA). p53 mutant p53 (G245D) , but not p53 (R249S) , directly bound to ZBP-89 and prevented its translocation from cytoplasm to nucleus. Furthermore, p53 (G245D) was shown to have a similar pattern of subcellular localization to ZBP-89 in tissues of HCC patients in Hong Kong. Functionally, the cytoplasmic accumulation of ZBP-89 by p53 (G245D) significantly abrogated the induction of p21 caused by sodium butyrate (NaB) treatment and protected cells from TSA-induced death. The activations of several apoptotic proteins, such as Bid and PARP, were involved in p53 (G245D) -m... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5578497 Wed, 11 Jan 2012 16:01:14 +0100 5578497 http://www.medworm.com/index.php?rid=5578496&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22214765%26dopt%3DAbstract Authors: Wanner SP, Garami A, Pakai E, Oliveira DL, Gavva NR, Coimbra CC, Romanovsky AA Abstract Studies in young rodents have shown that the transient receptor potential vanilloid-1 (TRPV1) channel plays a suppressive role in the systemic inflammatory response syndrome (SIRS) by inhibiting production of tumor necrosis factor (TNF)α and possibly by other mechanisms. We asked whether the anti-inflammatory role of TRPV1 changes with age. First, we studied the effect of AMG517, a selective and potent TRPV1 antagonist, on aseptic, lipopolysaccharide (LPS)-induced SIRS in young (12 wk) mice. In agreement with previous studies, AMG517 increased LPS-induced mortality in the young. We then studied the effects of TRPV1 antagonism (AMG517 or genetic deletion of TRPV1) on SIRS in middle-aged... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5578496 Wed, 11 Jan 2012 16:01:04 +0100 5578496 http://www.medworm.com/index.php?rid=5578495&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22214766%26dopt%3DAbstract Authors: Wang X, Sistrunk C, Miliani de Marval PL, Kim Y, Rodriguez-Puebla ML Abstract We have previously demonstrated that ras-mediated skin tumorigenesis depends on signaling pathways that act preferentially through cyclin D1 and D2. Interestingly, the expression of cyclin D3 inhibits skin tumor development, an observation that conflicts with the oncogenic role of D-type cyclins in the mouse epidermis. Here, we show that simultaneous up- and down-regulation of particular members of the D-type cyclin family is a valuable approach to reduce skin tumorigenesis. We developed the K5D3/cyclin D1 (-/-) compound mouse which overexpresses cyclin D3 but lacks expression of cyclin D1 in the skin. Similar to K5D3 transgenic mice, keratinocytes from K5D3/cyclin D1 (-/-) compound mice show a s... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5578495 Wed, 11 Jan 2012 16:00:53 +0100 5578495 http://www.medworm.com/index.php?rid=5578494&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22223094%26dopt%3DAbstract Authors: Razorenova OV Abstract Comment on: Khapre RV, et al. Cell Cycle 2011; 10:4162-9. PMID: 22223094 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5578494 Wed, 11 Jan 2012 16:00:42 +0100 5578494 http://www.medworm.com/index.php?rid=5578493&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22223095%26dopt%3DAbstract Authors: Borggrefe T, Liefke R Abstract Notch signaling plays a pivotal role in the regulation of many fundamental cellular processes, such as proliferation, stem cell maintenance and differentiation during embryonic and adult development. At the molecular level, ligand binding induces the proteolytic cleavage of the Notch receptor. The intracellular domain of Notch translocates subsequently into the nucleus, associates with the central transcription factor RBP-J and activates transcription. Although, this pathway is remarkably short, with no second messenger involved, it regulates expression of more than hundred target genes in a tissue-specific manner. This review summarizes recent studies on transcriptional and chromatin control mechanisms, which set the stage for specific expre... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5578493 Wed, 11 Jan 2012 16:00:32 +0100 5578493 http://www.medworm.com/index.php?rid=5578492&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22223138%26dopt%3DAbstract Authors: Yemelyanov A, Bhalla P, Yang X, Ugolkov A, Iwadate K, Karseladze A, Budunova I Abstract Androgen (AR) and glucocorticoid (GR) receptor signaling play opposing roles in prostate tumorigenesis: in prostate, AR acts as an oncogene, and GR is a tumor suppressor. Recently, we found that non-steroidal phyto-chemical Compound A (CpdA) is AR/GR modulator acting as anti-inflammatory anti-androgen. CpdA inhibits AR and prevents GR transactivation while enhancing GR transrepression. GR and AR are controlled by proteasomal degradation. We found that prolonged exposure of LNCaP, LNCaP-GR, DU145 and PC3 prostate carcinoma (PCa) cells to proteasome inhibitor Bortezomib (BZ) caused AR degradation and GR accumulation. BZ enhanced CpdA ability to inhibit AR and to augment GR transrepression... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5578492 Wed, 11 Jan 2012 16:00:22 +0100 5578492 http://www.medworm.com/index.php?rid=5550352&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22193033%26dopt%3DAbstract Authors: Shah JV Abstract Comment on: Delaval B, et al. Cell Cycle 2011; 10:3964-72. PMID: 22193033 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5550352 Thu, 29 Dec 2011 23:30:59 +0100 5550352 http://www.medworm.com/index.php?rid=5550351&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22193034%26dopt%3DAbstract Authors: Manolio TA, Chanock SJ Abstract Comment on: Glinskii AB, et al. Cell Cycle 2011; 10:3571-97. PMID: 22193034 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5550351 Thu, 29 Dec 2011 23:30:48 +0100 5550351 http://www.medworm.com/index.php?rid=5550350&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22193035%26dopt%3DAbstract Authors: Costa V, Ludovico P Abstract Comment on: Carmona-Gutierrez D, et al. Cell Cycle 2011; 10:3973-8. PMID: 22193035 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5550350 Thu, 29 Dec 2011 23:30:36 +0100 5550350 http://www.medworm.com/index.php?rid=5550349&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22193036%26dopt%3DAbstract Authors: Harris AL Abstract Comment on: Diana Whitaker-Menezes D, et al. Cell Cycle 2011; 10:4047-64. PMID: 22193036 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5550349 Thu, 29 Dec 2011 23:30:25 +0100 5550349 http://www.medworm.com/index.php?rid=5550348&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22193044%26dopt%3DAbstract Authors: Rossetti S, Esposito J, Corlazzoli F, Gergorski A, Sacchi N Abstract Most physiological and biological processes are regulated by endogenous circadian rhythms under the control of both a master clock, which acts systemically and individual cellular clocks, which act at the single cell level. The cellular clock is based on a network of core clock genes, which drive the circadian expression of non-clock genes involved in many cellular processes. Circadian deregulation of gene expression has emerged to be as important as deregulation of estrogen signaling in breast tumorigenesis. Whether there is a mutual deregulation of circadian and hormone signaling is the question that we address in this study. Here we show that, upon entrainment by serum shock, cultured human mammary epi... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5550348 Thu, 29 Dec 2011 23:30:14 +0100 5550348 http://www.medworm.com/index.php?rid=5535153&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%2520%28%2522Cell%2520Cycle%2522%255Bta%255D%29%2520AND%2520%25222011%252F11%252F18%252018.48%2522%255BEDAT%255D%253A%25222011%252F12%252F23%252018.36%2522%255BEDAT%255D%29 114 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results: "Cell Cycle"[ta] These pubmed results were generated on 2011/12/23PubMed, a service of the National Library of Medicine, includes over 15 million citations for biomedical articles back to the 1950's. These citations are from MEDLINE and additional life science journals. PubMed includes links to many sites providing full text articles and other related resources. (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5535153 Fri, 23 Dec 2011 23:36:01 +0100 5535153 http://www.medworm.com/index.php?rid=5379981&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22033146%26dopt%3DAbstract Energy transfer in "parasitic" cancer metabolism: Mitochondria are the powerhouse and Achilles' heel of tumor cells. Cell Cycle. 2011 Dec 15;10(24) Authors: Martinez-Outschoorn UE, Pestell RG, Howell A, Nagajyothi F, Machado FS, Tanowitz HB, Sotgia F, Lisanti MP Abstract It is now widely recognized that the tumor microenvironment promotes cancer cell growth and metastasis via changes in cytokine secretion and extracellular matrix remodeling. However, the role of tumor stromal cells in providing energy for epithelial cancer cell growth is a newly emerging paradigm. For example, we and others have recently proposed that tumor growth and metastasis is related to an energy imbalance. Host cells produce energy-rich nutrients via catabolism (through autophagy, mitophagy, and aero... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379981 Sun, 06 Nov 2011 20:29:57 +0100 5379981 http://www.medworm.com/index.php?rid=5380015&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22024914%26dopt%3DAbstract Authors: Iwasaki O, Corcoran CJ, Noma KI Abstract Comment on: Wang J, et al. Cell Cycle 2011; 10:3016-30. PMID: 22024914 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5380015 Tue, 01 Nov 2011 04:00:00 +0100 5380015 http://www.medworm.com/index.php?rid=5380014&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22024915%26dopt%3DAbstract Authors: Mazzoni C, Falcone C Abstract Comment on: Scheckhuber CQ, et al. Cell Cycle 2011; 10:3105-10. PMID: 22024915 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5380014 Tue, 01 Nov 2011 04:00:00 +0100 5380014 http://www.medworm.com/index.php?rid=5380013&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22024916%26dopt%3DAbstract Authors: Cheng CY, Nikitin AY Abstract Comment on: Park KS, et al. Cell Cycle 2011; 10:2806-15. PMID: 22024916 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5380013 Tue, 01 Nov 2011 04:00:00 +0100 5380013 http://www.medworm.com/index.php?rid=5380012&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22024917%26dopt%3DAbstract Authors: Hang LE, Zhao X Abstract Comment on: Parnas O, et al. Cell Cycle 2011; 10:2894-903. PMID: 22024917 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5380012 Tue, 01 Nov 2011 04:00:00 +0100 5380012 http://www.medworm.com/index.php?rid=5380011&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22024918%26dopt%3DAbstract Authors: Goldstein AS, Huang J Abstract Comment on: Park K, et al. Cell Cycle 2011; 10:2140-50. PMID: 22024918 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5380011 Tue, 01 Nov 2011 04:00:00 +0100 5380011 http://www.medworm.com/index.php?rid=5379984&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22032922%26dopt%3DAbstract Authors: Sohr S, Engeland K Abstract Successful pregnancy requires a functionally normal blastocyst encountering a receptive maternal endometrium. Interestingly, the cell cycle regulator and tumor suppressor p53 has been reported to support reproduction in mice by regulating the expression of the leukemia inhibitory factor gene in the maternal endometrium. However, in humans the hormonal system orchestrating successful pregnancy is considerably different from rodents. Particularly, the primate-specific dimeric glycoprotein hormone human chorionic gonadotropin (hCG) is essential for blastocyst implantation and maintenance of early human pregnancy. Here we provide evidence that p53 selectively induces expression of the hCGbeta7 (CGB7) gene. None of the other CGB genes was found to be... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379984 Tue, 01 Nov 2011 04:00:00 +0100 5379984 http://www.medworm.com/index.php?rid=5379983&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22032989%26dopt%3DAbstract This study identifies CSA and CSB as the key elements of a regulatory mechanism that equilibrate beneficial and detrimental effects of p53 activity upon cellular stress. The deregulation of p53, in absence of either of the CS proteins, can potentially explain the early onset degeneration of tissues and organs observed in CS patients. PMID: 22032989 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379983 Tue, 01 Nov 2011 04:00:00 +0100 5379983 http://www.medworm.com/index.php?rid=5379982&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22033139%26dopt%3DAbstract Authors: Maekawa M, Yamanaka S Abstract Comment on: Maekawa M, et al. Nature 2011; 474:225-9. PMID: 22033139 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379982 Tue, 01 Nov 2011 04:00:00 +0100 5379982 http://www.medworm.com/index.php?rid=5379980&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22033176%26dopt%3DAbstract Authors: Charvet C, Maurer U Abstract Comment on: Charvet C, et al. Mol Cell 2011; 42:584-96. PMID: 22033176 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379980 Tue, 01 Nov 2011 04:00:00 +0100 5379980 http://www.medworm.com/index.php?rid=5379979&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22033177%26dopt%3DAbstract Authors: Hansell CA, Nibbs RJ Abstract Comment on: Hansell CA, et al. Blood 2011; 117:5413-24. PMID: 22033177 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379979 Tue, 01 Nov 2011 04:00:00 +0100 5379979 http://www.medworm.com/index.php?rid=5379978&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22033178%26dopt%3DAbstract Authors: Lee BH, Kang S Abstract Comment on: Elf S, et al. Blood 2011; 117:6885-94. PMID: 22033178 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379978 Tue, 01 Nov 2011 04:00:00 +0100 5379978 http://www.medworm.com/index.php?rid=5379977&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22033189%26dopt%3DAbstract Authors: Chang M, Rothstein R PMID: 22033189 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379977 Tue, 01 Nov 2011 04:00:00 +0100 5379977 http://www.medworm.com/index.php?rid=5379976&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22033190%26dopt%3DAbstract Authors: Eguiara A, Holgado O, Beloqui I, Abalde L, Sanchez Y, Callol C, Martin AG Abstract The cancer stem cell is defined by its capacity to self-renew, the potential to differentiate into all cells of the tumor and the ability to proliferate and drive the expansion of the tumor. Thus, targeting these cells may provide novel anti-cancer treatment strategies. Breast cancer stem cells have been isolated according to surface marker expression, ability to efflux fluorescent dyes, increased activity of aldehyde dehydrogenase or the capacity to form spheres in non-adherent culture conditions. In order to test novel drugs directed towards modulating self-renewal of cancer stem cells, rapid, easy and inexpensive assays must be developed. Using 2 days-post-fertilization (dpf) zebrafish em... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379976 Tue, 01 Nov 2011 04:00:00 +0100 5379976 http://www.medworm.com/index.php?rid=5379975&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22033214%26dopt%3DAbstract Authors: Destici E, Oklejewicz M, Saito S, van der Horst GT Abstract By gating cell cycle progression to specific times of the day, the intracellular circadian clock is thought to reduce the exposure of replicating cells to potentially hazardous environmental and endogenous genotoxic compounds. Although core clock gene defects that eradicate circadian rhythmicity can cause an altered in vivo genotoxic stress response and aberrant proliferation rate, it remains to be determined to what extent these cell cycle related phenotypes are due to a cell-autonomous lack of circadian oscillations. We investigated the DNA damage sensitivity and proliferative capacity of cultured primary Cry1 (‑/- ) (|) Cry2 (‑/-) fibroblasts. Contrasting previous in vivo studies, we show that the absence... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379975 Tue, 01 Nov 2011 04:00:00 +0100 5379975 http://www.medworm.com/index.php?rid=5379974&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22033215%26dopt%3DAbstract Authors: Kõivomägi M, Loog M Abstract Comment on: Kõivomägi M, et al. Mol Cell 2011; 42:610-23. PMID: 22033215 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379974 Tue, 01 Nov 2011 04:00:00 +0100 5379974 http://www.medworm.com/index.php?rid=5379973&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22033337%26dopt%3DAbstract Authors: Muñoz-Fontela C, González D, Marcos-Villar L, Campagna M, Gallego P, González-Santamaría J, Herranz D, Gu W, Serrano M, Aaronson SA, Rivas C Abstract Tumor suppressor p53 is known to be a direct transcriptional target of type I interferons (IFNs), contributing to virus-induced apoptosis, and in turn activating itself the interferon pathway. Acetylation, among many other post-translational modifications of p53, is thought to exert a crucial role regulating p53 activity. Here, we examined the contribution of this modification on the antiviral activity mediated by p53. Our results show that virus infection induces p53 acetylation at lysine 379, and that this modification is absolutely required for p53-dependent transcriptional transactivation of both, pro-apoptotic and IF... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379973 Tue, 01 Nov 2011 04:00:00 +0100 5379973 http://www.medworm.com/index.php?rid=5379972&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22033440%26dopt%3DAbstract Authors: Ricke RM, van Deursen JM Abstract High expression of the mitotic kinase Bub1 is associated with a variety of human cancers and correlates with poor clinical prognosis, but whether Bub1 alone can drive tumorigenesis was unknown. We provided conclusive evidence that Bub1 has oncogenic properties by generating transgenic mice that overexpress Bub1 in a wide variety of tissues, resulting in aneuploidization. Consistently, Bub1 transgenic mice developed various kinds of spontaneous tumors as well as accelerated Myc-induced lymphomagenesis. While the mitotic checkpoint was robust in Bub1 overexpressing cells, misaligned and lagging chromosomes were observed. These defects originated from increased Aurora B activity and could be suppressed by inhibition of Aurora B. Taken togethe... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379972 Tue, 01 Nov 2011 04:00:00 +0100 5379972 http://www.medworm.com/index.php?rid=5379971&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22037208%26dopt%3DAbstract Authors: Gentles AJ, Alizadeh AA Abstract Comment on: Alizadeh AA, et al. Blood. 2011; 118:1350-8. PMID: 22037208 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379971 Tue, 01 Nov 2011 04:00:00 +0100 5379971 http://www.medworm.com/index.php?rid=5379970&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22037209%26dopt%3DAbstract Systems biology of epistasis: Shedding light on genetic interaction network "hubs" Cell Cycle. 2011 Nov 1;10(21) Authors: Papp B, Pál C Abstract Comment on: Szappanos B, et al. Nat Genet 2011; 43:656-62. PMID: 22037209 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379970 Tue, 01 Nov 2011 04:00:00 +0100 5379970 http://www.medworm.com/index.php?rid=5379969&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22037210%26dopt%3DAbstract Authors: Ohno S, Shibayama M, Sato M, Tokunaga A, Yoshida N Abstract Polypyrimidine tract-binding protein (PTB/PTBP1/hnRNP I) is a member of the heterogeneous nuclear ribonucleoprotein family that binds specifically to pyrimidine-rich sequences of RNAs. Although PTB is a multifunctional protein involved in RNA processing and internal ribosome entry site (IRES)-dependent translation, the role of PTB in early mouse development is unclear. Ptb knockout mice exhibit embryonic lethality shortly after implantation and Ptb-/- embryonic stem (ES) cells have a severe proliferation defect that includes a prolonged G2/M phase. The present study shows that PTB promotes M phase progression by the direct repression of CDK11p58 IRES activity in ES cells. The protein expression and IRES activity o... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379969 Tue, 01 Nov 2011 04:00:00 +0100 5379969 http://www.medworm.com/index.php?rid=5379968&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22037211%26dopt%3DAbstract Authors: Tipton AR, Tipton M, Yen T, Liu ST Abstract The mitotic checkpoint is a specialized signal transduction pathway that monitors kinetochore-microtubule attachment to achieve faithful chromosome segregation. MAD2 is an evolutionarily conserved mitotic checkpoint protein that exists in open (O) and closed (C) conformations. The increase of intracellular C-MAD2 level during mitosis, through OC-MAD2 conversion as catalyzed by unattached kinetochores, is a critical signaling event for the mitotic checkpoint. However, it remains controversial whether MAD2 is an integral component of the effector of the mitotic checkpoint---the Mitotic Checkpoint Complex (MCC). We show here that endogenous human MCC is assembled by first forming a BUBR1:BUB3:CDC20 complex in G2 and then selectiv... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379968 Tue, 01 Nov 2011 04:00:00 +0100 5379968 http://www.medworm.com/index.php?rid=5379967&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22037254%26dopt%3DAbstract Authors: Ferretti R, Sbroggiò M, Di Savino A, Fusella F, Bertero A, Michowski W, Tarone G, Brancaccio M Abstract Chaperones and scaffold proteins are key elements involved in controlling the assembly of molecular complexes required for coordinated signal transduction. Here we describe morgana and melusin, two phylogenetically conserved chaperones that cooperate with Hsp90 and regulate signal transduction in important physiopathological processes. While morgana is ubiquitously expressed, melusin expression is restricted to striated muscles. Despite high sequence homology, the two chaperones have distinct functions. Morgana controls genomic stability by regulating the centrosome cycle via ROCKII kinase. Melusin, however, organizes ERK signal transduction in cardiomyocytes and regula... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379967 Tue, 01 Nov 2011 04:00:00 +0100 5379967 http://www.medworm.com/index.php?rid=5379966&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22037286%26dopt%3DAbstract Authors: Henderson A, Hershey JW Abstract Comment on: Henderson A, et al. Proc Natl Acad Sci USA 2011; 108:6415-9. PMID: 22037286 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379966 Tue, 01 Nov 2011 04:00:00 +0100 5379966 http://www.medworm.com/index.php?rid=5379965&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22037398%26dopt%3DAbstract Authors: Prendergast AM, Cruet-Hennequart S, Shaw G, Barry FP, Carty MP Abstract DNA damaging agents are widely used in treatment of hematogical malignancies and solid tumors. While effects on hematopoietic stem cells have been characterized, less is known about the DNA damage response in human mesenchymal stem cells (hMSCs) in the bone marrow stroma, progenitors of osteoblasts, chondrocytes and adipocytes. To elucidate the response of undifferentiated hMSCs to gamma-irradiation and cisplatin, key DNA damage responses have been characterised in hMSCs from normal adult donors. Cisplatin and gamma-irradiation activated the DNA damage response in hMSCs, including induction of p53 and p21, and activation of PI3 kinase-related protein kinase (PIKK)-dependent phosphorylation of histone H... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379965 Tue, 01 Nov 2011 04:00:00 +0100 5379965 http://www.medworm.com/index.php?rid=5379964&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22041584%26dopt%3DAbstract Authors: Salem AF, Bonuccelli G, Bevilacqua G, Arafat HA, Pestell RG, Sotgia F, Lisanti MP Abstract Pancreatic cancer is one of the deadliest cancers due to early rapid metastasis and chemoresistance. Recently, epithelial to mesenchymal transition (EMT) was shown to play a key role in the pathogenesis of pancreatic cancer. To understand the role of caveolin-1 (Cav-1) in EMT, we over-expressed Cav-1 in a pancreatic cancer cell line, Panc 10.05, that does not normally express Cav-1. Here, we show that Cav-1 expression in pancreatic cancer cells induces an epithelial phenotype and promotes cell-cell contact, with increased expression of plasma membrane bound E-cadherin and beta-catenin. Mechanistically, Cav-1 induces Snail downregulation and decreased activation of AKT, MAPK and TGF-b... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379964 Tue, 01 Nov 2011 04:00:00 +0100 5379964 http://www.medworm.com/index.php?rid=5379963&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22041656%26dopt%3DAbstract Authors: Siejka A, Barabutis N, Schally AV Abstract AMP-activated protein kinase (AMPK) regulates cellular proliferation, growth and metabolism. Targeted activation of AMPK is considered an important therapeutic strategy for cancer treatment. To evaluate the effect of growth hormone-releasing hormone (GHRH) and its antagonist MZ-5-156 on the phosphorylation of AMPK and other related regulatory intracellular proteins we employed human non-small cell lung cancer cell line A549, which expresses GHRH receptors. Treatment of A549 cells with GHRH antagonist decreased cell proliferation and activated AMPK as well as glycogen synthase kinase (GSK)3β. Furthermore, MZ-5-156 inhibited Akt, the mammalian target of rapamycin (mTOR) and its downstream target eIF4E which controls protein synthes... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379963 Tue, 01 Nov 2011 04:00:00 +0100 5379963 http://www.medworm.com/index.php?rid=5379962&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22041657%26dopt%3DAbstract Authors: Simsek D, Jasin M Abstract DNA ligases are crucial for most DNA transactions, including DNA replication, repair, and recombination. Recently, DNA ligase III (Lig3) has been demonstrated to be crucial for cell survival due to its catalytic function in mitochondria. This review summarizes these recent results and reports on a hitherto unappreciated widespread phylogenetic presence of Lig3 in eukaryotes, including in some organisms before the divergence of metazoa. Analysis of these putative Lig3 homologs suggests that many of them are likely to be found in mitochondria and to be critical for mitochondrial function. PMID: 22041657 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379962 Tue, 01 Nov 2011 04:00:00 +0100 5379962 http://www.medworm.com/index.php?rid=5379961&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22041711%26dopt%3DAbstract Authors: Vasudevan NT, Mohan ML, Goswami SK, Naga Prasad SV Abstract G protein-coupled receptors are the largest family of cell surface receptors regulating multiple cellular processes. β-adrenergic receptor (βAR) is a prototypical member of GPCR family and has been one of the most well studied receptors in determining regulation of receptor function. Agonist activation of βAR leads to conformational change resulting in coupling to G protein generating cAMP as secondary messenger. The activated βAR is phosphorylated resulting in binding of β-arrestin that physically interdicts further G protein coupling leading to receptor desensitization. The phosphorylated βAR is internalized and undergoes resensitization by dephosphorylation mediated by protein phosphatase 2A in the early ... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379961 Tue, 01 Nov 2011 04:00:00 +0100 5379961 http://www.medworm.com/index.php?rid=5379960&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22041817%26dopt%3DAbstract Authors: Forster N, Ellisen LW Abstract Comment on: Kent S, et al. Cell Cycle 2011; 10:3111-8. PMID: 22041817 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379960 Tue, 01 Nov 2011 04:00:00 +0100 5379960 http://www.medworm.com/index.php?rid=5379959&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22045038%26dopt%3DAbstract Authors: Kupsch C, Schmitz-Linneweber C Abstract Comment on: Lopez Sanchez MIG, et al. Cell Cycle 2011; 10:2904-16. PMID: 22045038 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379959 Tue, 01 Nov 2011 04:00:00 +0100 5379959 http://www.medworm.com/index.php?rid=5379958&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22045127%26dopt%3DAbstract Authors: Sun M, Hart JR, Hillmann P, Gymnopoulos M, Vogt PK Abstract Addition of short (6 to 16 amino acids) peptide sequences to the N-terminus of p110α induces a gain of function. Such sequences include the common Flag, His, and VSV tags as well as random sequences. An N-terminal myristylation signal generally believed to activate p110α by providing a constitutive membrane address is also activating, if myristylation is mutationally abolished. The gain of function seen with N-terminally tagged (NTT) p110α constructs extends to signaling, oncogenic transformation and stimulation of cell growth. The activating effect of N-terminal tags requires a functional Ras-binding domain in p110α. Mutations in that domain (T208D and K227A) abolish the gains of function in oncogenicity and ... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379958 Tue, 01 Nov 2011 04:00:00 +0100 5379958 http://www.medworm.com/index.php?rid=5379957&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22045204%26dopt%3DAbstract Authors: Redwood AB, Gonzalez-Suarez I, Gonzalo S Abstract Spatial and temporal organization of the genome represents an additional step in the regulation of nuclear functions. The nuclear lamina, a polymeric meshwork formed by lamins (A/C and B type) and lamin-associated proteins, plays a key role in the maintenance of genome localization, structure and function. Specifically, mutations in the LMNA gene -encoding lamins A/C- or changes in its expression -either upregulation or silencing- are associated with defects in DNA replication, transcription and repair, as well as alterations in epigenetic modifications of chromatin. These data, together with the fact that defects in A-type lamins are associated with a whole variety of degenerative disorders, premature aging syndromes and c... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379957 Tue, 01 Nov 2011 04:00:00 +0100 5379957 http://www.medworm.com/index.php?rid=5379956&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22052357%26dopt%3DAbstract This article reviews the existing research evidence that the most established mTOR inhibitors can notably decelerate the cellular senescence that is imposed by DNA damage-like responses, which are somewhat equivalent to the responses caused by reprogramming factors. These data suggest that fine-tuning mTOR signaling can impact mitochondrial dynamics to segregate mitochondria that are destined for clearance through autophagy, which results in the loss of mitochondrial function and in the accelerated onset of the glycolytic metabolism that is required to fuel reprogramming. By critically exploring how mTOR-regulated senescence, bioenergetic infrastructure and autophagy can actively drive the reprogramming of somatic cells to pluripotency, we define a metabolic roadmap that may be helpful for... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379956 Tue, 01 Nov 2011 04:00:00 +0100 5379956 http://www.medworm.com/index.php?rid=5379955&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22052358%26dopt%3DAbstract Authors: Del Galdo F Abstract Comment  on: Castello-Cros R, et al. Cell Cycle 2011; 10:2140-50. PMID: 22052358 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379955 Tue, 01 Nov 2011 04:00:00 +0100 5379955 http://www.medworm.com/index.php?rid=5379954&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22052359%26dopt%3DAbstract Conclusions: The downstream response to DNA damage in p53 wild-type neuroblastoma cell lines is p53 dependent, and determined both by the morphological sub-type and MYCN expression. PMID: 22052359 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379954 Tue, 01 Nov 2011 04:00:00 +0100 5379954 http://www.medworm.com/index.php?rid=5380010&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22024923%26dopt%3DAbstract Authors: Janes KA Abstract The transcription factor Runt-related transcription factor 1 (RUNX1) is critical for the earliest steps of hematopoiesis. RUNX1 was originally identified as a gene fusion in acute myeloid leukemia (AML) and thus has garnered heavy attention as a tumor suppressor in hematopoietic malignancies. However, RUNX1 is also strongly expressed in breast epithelia and may be misregulated during tumorigenesis. Here, I discuss our recent work implicating RUNX1 in proliferation control during breast epithelial-acinar morphogenesis. My goal is to place these findings in the context of a handful of other reports, which together argue that RUNX1 could act as a tumor suppressor gene in breast cancer. Testing this hypothesis requires focused in vivo studies, because the maj... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5380010 Mon, 31 Oct 2011 04:00:00 +0100 5380010 http://www.medworm.com/index.php?rid=5380009&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22024924%26dopt%3DAbstract Authors: Rosner M, Hengstschläger M PMID: 22024924 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5380009 Mon, 31 Oct 2011 04:00:00 +0100 5380009 http://www.medworm.com/index.php?rid=5380008&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22024925%26dopt%3DAbstract Authors: Florian S, Mayer TU Abstract Activity of the sliding motor Eg5 and coordinated microtubule dynamics are both essential for mitotic spindle pole separation. It is still a matter of controversy if changes in microtubule dynamics can compensate inhibition of Eg5 activity and re-enable bipolarization. Using a consistent live-cell-imaging approach, we show that perturbation of microtubule dynamics can compensate inhibition of Eg5 through a spindle formation process reminiscent of meiosis: In Eg5-inhibited mammalian somatic cells, alteration of microtubule dynamics through depletion of TOGp or low doses of nocodazole induces the formation of multiple acentrosomal spindle poles which pass through an intermediate multipolar state followed by bipolarization. Pole separation depends... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5380008 Mon, 31 Oct 2011 04:00:00 +0100 5380008 http://www.medworm.com/index.php?rid=5380007&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22024926%26dopt%3DAbstract Authors: Chen BB, Glasser JR, Coon TA, Mallampalli RK Abstract Mitotic progression is regulated by ubiquitin E3 ligase complexes to carefully orchestrate eukaryotic cell division. Here we show that a relatively new E3 ligase component belonging to the SCF (Skip-Cullin1-F-box protein) E3 ligase family, SCF (FBXL2) , impairs cell proliferation by mediating cyclin D3 polyubiquitination and degradation. Both cyclin D3 and FBXL2 co-localize within the centrosome. FBXL2 overexpression led to G2/M phase arrest in transformed epithelia resulting in appearance of supernumerary centrosomes, tetraploidy, and nuclei where condensed chromosomes are arranged on circular monopolar spindles typical of mitotic arrest.  RNAi mediated knockdown of cyclin D3 recapitulated effects of SCF (FBXL2) expre... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5380007 Mon, 31 Oct 2011 04:00:00 +0100 5380007 http://www.medworm.com/index.php?rid=5380006&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22024927%26dopt%3DAbstract Authors: McCulley J, Myung K Abstract Comment on: Parnas O, et al. Cell Cycle 2011; 10:2894-903. PMID: 22024927 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5380006 Mon, 31 Oct 2011 04:00:00 +0100 5380006 http://www.medworm.com/index.php?rid=5380005&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22024928%26dopt%3DAbstract Authors: Speroni J, Gottifredi V Abstract Comment on: Ciznadija D, et al. Cell Cycle 2011; 10:2714-23. PMID: 22024928 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5380005 Mon, 31 Oct 2011 04:00:00 +0100 5380005 http://www.medworm.com/index.php?rid=5380004&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22024929%26dopt%3DAbstract Authors: Fearon E Abstract Comment on: Nagano Y, et al. Cell Cycle 2011; 10:2593-603. PMID: 22024929 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5380004 Mon, 31 Oct 2011 04:00:00 +0100 5380004 http://www.medworm.com/index.php?rid=5380003&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22024930%26dopt%3DAbstract Authors: Palmero I Abstract Comment on: Ferrer I, et al. Cell Cycle 2011; 10:2751-62. PMID: 22024930 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5380003 Mon, 31 Oct 2011 04:00:00 +0100 5380003 http://www.medworm.com/index.php?rid=5380002&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22024931%26dopt%3DAbstract Authors: Brachner A, Foisner R Abstract Comment on: Redwood AB, et al. Cell Cycle 2011; 10:2550-61. PMID: 22024931 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5380002 Mon, 31 Oct 2011 04:00:00 +0100 5380002 http://www.medworm.com/index.php?rid=5380001&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22024932%26dopt%3DAbstract Authors: Darzynkiewicz Z Abstract Comment on: Ciznadija D, et al. Cell Cycle 2011; 10:2714-23. PMID: 22024932 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5380001 Mon, 31 Oct 2011 04:00:00 +0100 5380001 http://www.medworm.com/index.php?rid=5380000&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22030465%26dopt%3DAbstract Authors: Macpherson D Abstract Comment on: Park K, et al. Cell Cycle 2011; 10:2806-15. PMID: 22030465 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5380000 Mon, 31 Oct 2011 04:00:00 +0100 5380000 http://www.medworm.com/index.php?rid=5379999&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22030554%26dopt%3DAbstract Authors: Tehrani Z, Lin S Abstract Type 1 diabetes results from the autoimmune destruction of insulin-producing pancreatic β cells. Current efforts to cure diabetes are aimed at replenishing damaged cells by generating a new supply of β cells in vitro. The most promising strategy for achieving this goal is to differentiate embryonic stem (ES) cells by sequentially exposing them to signaling molecules that they would normally encounter in vivo. This approach requires a thorough understanding of the temporal sequence of the signaling events underlying pancreatic β-cell induction during embryonic development. The zebrafish system has emerged as a powerful tool in the study of pancreas development. In this review, we provide a temporal summary of pancreas development in zebrafish wi... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379999 Mon, 31 Oct 2011 04:00:00 +0100 5379999 http://www.medworm.com/index.php?rid=5379998&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22030559%26dopt%3DAbstract Authors: Huang H, Ma YF, Bao Y, Lee H, Lisanti MP, Tanowitz HB, Weiss LM Abstract Toxoplasma gondii is an obligate intracellular protozoan that is both a human and animal pathogen. This Apicomplexan causes significant morbidity and mortality in immune competent and immune compromised hosts. In humans, the most common manifestations of T. gondii infections are chorioretinitis in congenital infection and encephalitis in immune compromised patients such as patients with advanced AIDS. Mitogen-activated protein kinase (MAPK) pathways are major signal transduction systems by which eukaryotic cells convert environmental cues to intracellular events such as proliferation and differentiation. We have identified a T. gondii homologue of the MAPK family that we have called TgMAPK2. Sequence ... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379998 Mon, 31 Oct 2011 04:00:00 +0100 5379998 http://www.medworm.com/index.php?rid=5379997&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22030621%26dopt%3DAbstract Authors: Höglund A, Strömvall K, Li Y, Forshell LP, Nilsson JA Abstract Myc is a transcription factor frequently found deregulated in human cancer. The Myc-mediated cellular transformation process is associated with fast proliferative cells and inherent genomic instability, giving rise to malignant, invasive neoplasms with poor prognosis for survival. Transcription-independent functions of Myc include stimulation of replication. Excessive Myc expression stimulates a replication-associated DNA damage response that signal via the phosphoinositide 3-kinase (PI3K) related protein kinases (PIKKs) ATM and ATR. These in turn activate the DNA damage transducers Chk1 and Chk2. Here, we show that Myc can stimulate Chek2 transcript indirectly in vitro, as well as in B cells of λ-Myc transg... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379997 Mon, 31 Oct 2011 04:00:00 +0100 5379997 http://www.medworm.com/index.php?rid=5379996&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22030622%26dopt%3DAbstract Authors: Czerwoniec A, Bujnicki JM Abstract Cytoplasmic initiator tRNAs from plants and fungi are excluded from participating in translational elongation by the presence of a unique 2'-phosphoribosyl modification of purine 64, introduced posttranscriptionally by the enzyme Rit1p. Members of the Rit1p family show no obvious similarity to other proteins or domains, there is no structural information available to guide experimental analyses, and the mechanism of action of this enzyme remains a mystery. Using protein fold-recognition we identified a phosphatase-like domain in the C-terminal part of Rit1p. A comparative model of the C-terminal domain was constructed and used to predict the function of conserved residues and to propose the mechanism of action of Rit1p. The model will fac... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379996 Mon, 31 Oct 2011 04:00:00 +0100 5379996 http://www.medworm.com/index.php?rid=5379995&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22030623%26dopt%3DAbstract Authors: Knoll S, Fürst K, Thomas S, Villanueva Baselga S, Stoll A, Schaefer S, Pützer BM Abstract Chronic hepatitis B virus (HBV) infection is the major risk for hepatocellular carcinomas (HCC). HBV X protein (HBx) and p53 tumor suppressor family interactions may be crucial for HCC induction. We compared p53 and p73 interactions with HBx in normal and HCC tumor cell lines differing in their p53 status. In the latter, HBx was pro-apoptotic, but exhibited opposite effects in non-tumor cells. In these normal cells, p53 and p73 were retained in the cytoplasm. In hepatoma cells, however, HBx led to nuclear translocation of p53 and p73 followed by enhanced transactivation of p53-dependent promoters. The nuclear transfer of p53, but not of p73, was abrogated by protein kinase C inhibit... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379995 Mon, 31 Oct 2011 04:00:00 +0100 5379995 http://www.medworm.com/index.php?rid=5379994&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22030624%26dopt%3DAbstract Authors: Zhang Z, Yang Z, Jäämaa S, Liu H, Pellakuru LG, Iwata T, Af Hällström TM, De Marzo AM, Laiho M Abstract The ability of cells to respond and repair DNA damage is fundamental for the maintenance of genomic integrity. Ex vivo-culturing of surgery-derived human tissues has provided a significant advancement to assess DNA damage response (DDR) in the context of normal cytoarchitecture in a non-proliferating tissue. Here we assess the dependency of prostate epithelium DDR on ATM and DNA-PKcs, the major kinases responsible for damage detection and repair by non-homologous end-joining (NHEJ), respectively. DNA damage was caused by ionizing radiation (IR) and cytotoxic drugs, cultured tissues were treated with ATM and DNA-PK inhibitors, and DDR was assessed by phosphorylation o... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379994 Mon, 31 Oct 2011 04:00:00 +0100 5379994 http://www.medworm.com/index.php?rid=5379993&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22030625%26dopt%3DAbstract Authors: Furuta S, Ghajar CM, Bissell MJ Abstract Comment on: Witkiewicz AK, et al. Cell Cycle 2011; 10:1794-809. PMID: 22030625 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379993 Mon, 31 Oct 2011 04:00:00 +0100 5379993 http://www.medworm.com/index.php?rid=5379992&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22030692%26dopt%3DAbstract Authors: Sarkar D, Wang XY, Fisher PB Abstract Comment on: Zerbini LF, et al. Cell Cycle 2011; 10:2583-91. PMID: 22030692 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379992 Mon, 31 Oct 2011 04:00:00 +0100 5379992 http://www.medworm.com/index.php?rid=5379991&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22030693%26dopt%3DAbstract Authors: Liebermann DA, Hoffman B Abstract Comment on: Zerbini L, et al. Cell Cycle 2011; 10: 2584-92. PMID: 22030693 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379991 Mon, 31 Oct 2011 04:00:00 +0100 5379991 http://www.medworm.com/index.php?rid=5379990&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22030861%26dopt%3DAbstract Authors: Cipak L, Zhang C, Kovacikova I, Rumpf C, Miadokova E, Shokat KM, Gregan J Abstract The genome of the fission yeast Schizosaccharomyces pombe encodes for 17 protein kinases that are essential for viability. Studies of the essential kinases often require the use of conditional alleles. To inactivate these kinases conditionally, we applied a recently developed chemical-genetic strategy. The mutation of a single residue in the ATP-binding pocket confers sensitivity to small-molecule inhibitors, allowing for specific inactivation of the modified kinase. Using this approach, we constructed conditional analog-sensitive alleles of 13 essential protein kinases in the fission yeast S. pombe. PMID: 22030861 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379990 Mon, 31 Oct 2011 04:00:00 +0100 5379990 http://www.medworm.com/index.php?rid=5379989&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22031019%26dopt%3DAbstract Authors: Kari V, Shchebet A, Neumann H, Johnsen SA Abstract Many anticancer therapies function largely by inducing DNA double-strand breaks (DSBs) or altering the ability of cancer cells to repair them. Proper and timely DNA repair requires dynamic changes in chromatin assembly and disassembly characterized by histone H3 lysine 56 acetylation (H3K56ac) and phosphorylation of the variant histone H2AX (γH2AX). Similarly, histone H2B monoubiquitination (H2Bub1) functions in DNA repair, but its role in controlling dynamic changes in chromatin structure following DSBs and the histone chaperone complexes involved remain unknown. Therefore, we investigated the role of the H2B ubiquitin ligase RNF40 in the DSB response. We show that RNF40 depletion results in sustained H2AX phosphorylatio... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379989 Mon, 31 Oct 2011 04:00:00 +0100 5379989 http://www.medworm.com/index.php?rid=5379988&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22031102%26dopt%3DAbstract Authors: Zhang L, Hu JJ, Gong F Abstract The 26S proteasome, a multicatalytic enzyme complex, is the main intracellular proteolytic system involved in the degradation of ubiquitinated proteins. The ability of proteasome inhibitors to induce apoptosis has been exploited in the recent development of chemotherapeutic agents. Here, we show that inhibition of proteasome by MG132 blocks DNA damage-induced apoptosis. Blockage of apoptosis by MG132 correlates with p53 stabilization and upregulation of p21/WAF1, a p53 transcriptional target. Surprisingly, in the absence of MG132, robust apoptosis induced by a high dose of UV irradiation correlate with rapid p53 degradation. This is in sharp contrast to p53 stabilization when cells were exposed to lower levels of UV irradiation. Our findings... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379988 Mon, 31 Oct 2011 04:00:00 +0100 5379988 http://www.medworm.com/index.php?rid=5379987&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22031223%26dopt%3DAbstract Authors: Brina D, Grosso S, Miluzio A, Biffo S Abstract Ribosome biogenesis and translation can be simplified as the processes of generating ribosomes and their use for decoding mRNA into a protein. Ribosome biogenesis has been efficiently studied in unicellular organisms like the budding yeast, allowing us a deep and basic knowledge of this process in growing cells. Translation has been modeled in vitro and in unicellular organisms. These studies have given us an important insight on the mechanisms and evolutionarily conserved aspects of ribosome biology. However, we advocate the need of the direct study of these processes in multicellular organisms. Analysis of ribosome biogenesis and translation, in vivo, in Metazoa and mammalian models is emerging and unveils the unexpected con... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379987 Mon, 31 Oct 2011 04:00:00 +0100 5379987 http://www.medworm.com/index.php?rid=5379986&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22031224%26dopt%3DAbstract Authors: Jones MH, Keck JM, Wong CC, Xu T, Yates JR, Winey M Abstract Phosphorylation of proteins is an important mechanism used to regulate most cellular processes. Recently we completed an extensive phosphoproteomic analysis of the core proteins that constitute the Saccharomyces cerevisiae centrosome. Here we present a study of phosphorylation sites found on the mitotic exit network (MEN) proteins, most of which are associated with the cytoplasmic face of the centrosome. We identified 55 sites on Bfa1, Cdc5, Cdc14, and Cdc15. Eight sites lie in cyclin-dependent kinase motifs (Cdk, S/T-P), and 22 sites are completely conserved within fungi. More than half of the sites were found in centrosomes from mitotic cells, possibly in preparation for their roles in mitotic exit. Finally, we... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379986 Mon, 31 Oct 2011 04:00:00 +0100 5379986 http://www.medworm.com/index.php?rid=5379985&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22031225%26dopt%3DAbstract Authors: Campos-Sanchez E, Toboso-Navasa A, Romero-Camarero I, Barajas-Diego M, Sanchez-García I, Cobaleda C Abstract The latest scientific findings in the field of cancer research are redefining our understanding of the molecular and cellular basis of the disease, moving the emphasis towards the study of the mechanisms underlying the alteration of the normal processes of cellular differentiation. The concepts best exemplifying this new vision are those of cancer stem cells and tumoral reprogramming. The study of the biology of acute lymphoblastic leukemias (ALLs) has provided seminal experimental evidences supporting these new points of view. Furthermore, in the case of B-cells, it has been shown that all the stages of their normal development show a tremendous degree of plastici... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5379985 Mon, 31 Oct 2011 04:00:00 +0100 5379985 http://www.medworm.com/index.php?rid=5297723&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%2520%28%2522Cell%2520Cycle%2522%255Bta%255D%29%2520AND%2520%25222011%252F10%252F04%252002.44%2522%255BEDAT%255D%253A%25222011%252F10%252F09%252006.05%2522%255BEDAT%255D%29 107 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results: "Cell Cycle"[ta] These pubmed results were generated on 2011/10/09PubMed, a service of the National Library of Medicine, includes over 15 million citations for biomedical articles back to the 1950's. These citations are from MEDLINE and additional life science journals. PubMed includes links to many sites providing full text articles and other related resources. (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5297723 Sun, 09 Oct 2011 10:05:01 +0100 5297723 http://www.medworm.com/index.php?rid=5281279&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21941082%26dopt%3DAbstract Authors: Srikantan S, Gorospe M, Abdelmohsen K Abstract Comment on: Marasa BS, et al. Aging 2010; 2:333-43. PMID: 21941082 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281279 Sat, 01 Oct 2011 04:00:00 +0100 5281279 http://www.medworm.com/index.php?rid=5281278&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21941083%26dopt%3DAbstract Authors: Ye F, Gao SJ Abstract Reactivation of Kaposi sarcoma-associated herpesvirus (KSHV) from latency for lytic replication plays a pivotal role in the development of KS tumors. However, the physiological factors of KSHV reactivation in KS patients remain undefined. Two recent studies independently discovered that the reactive oxygen species (ROS) H2O2 induces KSHV reactivation in latently infected cells, which can be inhibited by H2O2-specific antioxidants. H2O2 not only directly induces KSHV reactivation but also is involved in spontaneous lytic replication as well as reactivation stimulated by TPA, hypoxia, and cytokines. Furthermore, in a xenograft-based primary effusion lymphoma (PEL) mouse model, in vivo KSHV reactivation is also H2O2-dependent and can be suppressed by ant... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281278 Sat, 01 Oct 2011 04:00:00 +0100 5281278 http://www.medworm.com/index.php?rid=5281277&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21941084%26dopt%3DAbstract Authors: Macquarrie KL, Tapscott SJ Abstract Comment on: Lee, et al. Cancer Res 2011; 71:3921-31. PMID: 21941084 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281277 Sat, 01 Oct 2011 04:00:00 +0100 5281277 http://www.medworm.com/index.php?rid=5281276&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21941085%26dopt%3DAbstract In this report, we show the simultaneous phosphorylation and mitotic redistribution of a whole class of modified transcription factors. C2H2 zinc finger proteins (ZFPs) represent the largest group of gene expression regulators in the human genome. Despite their diversity, C2H2 ZFPs display striking conservation of small linker peptides joining their adjacent zinc finger modules. These linkers are critical for DNA binding activity. It has been proposed that conserved phosphorylation of these linker peptides could be a common mechanism for the inactivation of the DNA binding activity of C2H2 ZFPs, during mitosis. Using a novel antibody, raised against the phosphorylated form of the most conserved linker peptide sequence, we are able to visualize the massive and simultaneous mitotic phosphory... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281276 Sat, 01 Oct 2011 04:00:00 +0100 5281276 http://www.medworm.com/index.php?rid=5281275&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21941086%26dopt%3DAbstract Authors: Li H, Lakshmikanth T, Garofalo C, Enge M, Spinnler C, Anichini A, Szekely L, Kärre K, Carbone E, Selivanova G Abstract Escape of tumor cells from cell-intrinsic barrier mediated by tumor suppressors and cell-extrinsic barrier mediated by the immune system is crucial for tumorigenesis. Growing evidence suggests that reactivation of tumor suppressor function or restoration of anticancer immunity is promising strategy for anticancer therapy due to their high potential to combat cancer. p53, a key tumor suppressor, represses tumorigenesis by eliciting growth arrest, apoptosis or senescence in cancer cells. Here, we unravel that, apart from these cell-autonomous effects, p53 activates the innate immune response against cancer cells. Our results show that pharmacological reacti... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281275 Sat, 01 Oct 2011 04:00:00 +0100 5281275 http://www.medworm.com/index.php?rid=5281274&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21941087%26dopt%3DAbstract Authors: Pandit B, Gartel AL Abstract Apoptosis has been widely accepted as the primary mechanism of drug-induced cell death. Recently, a second type of cell death pathway has been demonstrated: autophagy, also called programmed type II cell death. Autophagy is a highly regulated process, by which selected components of a cell are degraded. It primarily functions as a cell survival mechanism under stress. However, persistent stress can also promote extensive autophagy leading to cell death. Forkhead box M1 (FoxM1), an oncogenic transcription factor that is abundantly expressed in a wide range of human cancers. Here we evaluated the role of FoxM1 in sensitivity of human cancer cells to proteasome inhibitor-induced apoptosis and autophagy. We found that FoxM1 knockdown sensitized the... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281274 Sat, 01 Oct 2011 04:00:00 +0100 5281274 http://www.medworm.com/index.php?rid=5281273&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21946516%26dopt%3DAbstract Authors: Guglielmino MR, Santonocito M, Vento M, Ragusa M, Barbagallo D, Borzì P, Casciano I, Banelli B, Barbieri O, Astigiano S, Scollo P, Romani M, Purrello M, Di Pietro C Abstract Studies on oocyte transcriptome are important to understand the biological pathways involved in oogenesis, totipotence and early embryonic development. Moreover, genes regulating physiological pathways in gametes could represent potential candidates for reproductive disorders. In addition to oocyte specific transcription factors, also the members of the p53 family could be etiologically involved due to their biological functions. In fact, their role in the control of cell cycle, apoptosis, and germ-line genome stability is well known. Female reproductive aging is one of  the causes of fertility reduc... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281273 Sat, 01 Oct 2011 04:00:00 +0100 5281273 http://www.medworm.com/index.php?rid=5281272&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21946517%26dopt%3DAbstract "Micromanaging" metabolic syndrome. Cell Cycle. 2011 Oct 1;10(19) Authors: Ramírez CM, Goedeke L, Fernández-Hernando C Abstract Metabolic diseases are characterized by the failure of regulatory genes or enzymes to effectively orchestrate specific pathways involved in the control of many biological processes. In addition to the classical regulators of metabolic homeostasis, recent discoveries have shown the remarkable role of small non-coding RNAs (microRNAs) in the post-transcriptional regulation of a number of genes, and their involvement in many pathological states, such as diabetes, atherosclerosis and cancer. Of note is microRNA-33 (miR-33), an intronic microRNA (miRNA) located within the sterol regulatory element-binding protein (SREBP) genes, one of the master regul... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281272 Sat, 01 Oct 2011 04:00:00 +0100 5281272 http://www.medworm.com/index.php?rid=5281271&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21946518%26dopt%3DAbstract Authors: Freije JM, Pendás AM Abstract Comment on: Redwood AB, et al. Cell Cycle 2011; 10:2549-60. PMID: 21946518 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281271 Sat, 01 Oct 2011 04:00:00 +0100 5281271 http://www.medworm.com/index.php?rid=5281270&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21946519%26dopt%3DAbstract Authors: Zhang J, Chen X Abstract Comment on: Park HK, et al. Cell Cycle 2011; 10:2574-82. PMID: 21946519 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281270 Sat, 01 Oct 2011 04:00:00 +0100 5281270 http://www.medworm.com/index.php?rid=5281269&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21946520%26dopt%3DAbstract Authors: Wang JY Abstract Comment on: Simonatto M, et al. Cell Cycle 2011; 10:2355-63. PMID: 21946520 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281269 Sat, 01 Oct 2011 04:00:00 +0100 5281269 http://www.medworm.com/index.php?rid=5281268&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21946521%26dopt%3DAbstract Authors: Sackett DL, Fojo T Abstract Comment on: Risinger AL, et al. Cell Cycle 2011; 10:2162-71. PMID: 21946521 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281268 Sat, 01 Oct 2011 04:00:00 +0100 5281268 http://www.medworm.com/index.php?rid=5281267&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21946522%26dopt%3DAbstract Authors: Spruck C Abstract Comment on: Lerner M, et al. Cell Cycle 2011; 10:2172-83. PMID: 21946522 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281267 Sat, 01 Oct 2011 04:00:00 +0100 5281267 http://www.medworm.com/index.php?rid=5281266&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21946523%26dopt%3DAbstract Authors: Iozzo RV Abstract Comment on: Castello-Cros R, et al. Cell Cycle 2011; 10:2021-34. PMID: 21946523 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281266 Sat, 01 Oct 2011 04:00:00 +0100 5281266 http://www.medworm.com/index.php?rid=5281265&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21946524%26dopt%3DAbstract Authors: Mukherjee B, Burma S Abstract Comment on: Fraser M, et al. Cell Cycle 2011; 10:2218-32. PMID: 21946524 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281265 Sat, 01 Oct 2011 04:00:00 +0100 5281265 http://www.medworm.com/index.php?rid=5281264&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21946569%26dopt%3DAbstract Authors: Golding SE, Valerie K Abstract Comment on: Fraser, M, et al. Cell Cycle 2011; 10:2218-32. PMID: 21946569 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281264 Sat, 01 Oct 2011 04:00:00 +0100 5281264 http://www.medworm.com/index.php?rid=5281263&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21952639%26dopt%3DAbstract Authors: Mori T, Ikeda DD, Fukushima T, Takenoshita S, Kochi H Abstract In biological networks, a small number of "hub" proteins play critical roles in the network integrity and functions. The cell cycle network orchestrates versatile cellular functions through interactions between many signaling modules, whose defects impair diverse cellular processes, often leading to cancer. However, the network architecture and molecular basis that ensure proper coordination between distinct modules is unclear. Here, we show that the ubiquitin ligase NIRF (also known as UHRF2), which induces G1 arrest, interacts with multiple cell cycle proteins including cyclins (A2, B1, D1 and E1), p53 and pRB, and ubiquitinates cyclins D1 and E1. Consistent with its versatility, a bioinformatic network analy... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281263 Sat, 01 Oct 2011 04:00:00 +0100 5281263 http://www.medworm.com/index.php?rid=5281262&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21957489%26dopt%3DAbstract Authors: Wani R, Tsang AW, Furdui CM Abstract Phosphorylation has long been recognized as the key mediator of protein signaling. New modes of signaling regulation are emerging with the development of specific chemical probes and application of high-throughput mass spectrometry technologies. Using biotin-tagged chemical probes for protein oxidation, mass spectrometry and functional assays, our group has recently reported isoform-specific oxidation of Akt2 in response to PDGF signaling. The studies included here investigate the functional consequence of oxidation on Akt2-mediated cell migration and cell cycle. Akt2-KO MEFs transduced with WT and Cys124Ser Akt2 were used as the model system for these studies. The implications of these findings on disease pathology are discussed. P... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281262 Sat, 01 Oct 2011 04:00:00 +0100 5281262 http://www.medworm.com/index.php?rid=5281261&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21957490%26dopt%3DAbstract Authors: Abbas HA, Pant V, Lozano G Abstract Hematopoietic stem cells provide an indispensible source for replenishing the blood with all its constituents throughout the organism's lifetime. Mice with a compromised hematopoietic stem cell compartment cannot survive. p53, a major tumor suppressor gene, has been implicated in regulation of hematopoiesis. In particular, p53 plays a role in homeostasis by regulating HSC quiescence and self renewal. We recently utilized a hypomorphic p53 ( 515C) allele in conjunction with Mdm2, a negative regulator of p53 to gain insights into the role of p53 in hematopoietic regulation. Our analyses revealed that p53 ( 515C/515C) Mdm2 (-/-) double mutant mice die soon after birth due to hematopoietic failure. Further mechanistic studies revealed that i... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281261 Sat, 01 Oct 2011 04:00:00 +0100 5281261 http://www.medworm.com/index.php?rid=5281260&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21957491%26dopt%3DAbstract Authors: Pluchino S, Alfaro-Cervello C Abstract Comment on: Russo I, et al. Cell Cycle 2011; 10:2218-32. PMID: 21957491 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281260 Sat, 01 Oct 2011 04:00:00 +0100 5281260 http://www.medworm.com/index.php?rid=5281259&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21957492%26dopt%3DAbstract Authors: Abou-Kandil A, Chamias R, Huleihel M, Godbey W, Aboud M Abstract Abstract Adult T-cell leukemia (ATL) is caused by HTLV-I. The viral Tax oncoprotein plays a central role in initiating the process to ATL. However, after infection HTLV-1 enters into latency, during which virus gene expression is very low, so that the level of Tax is likely insufficient for exerting its oncogenic activities. Therefore only 5% of the infected individuals may develop ATL several decades after infection. It is assumed that the transition from latency to ATL development requires at least a temporary activation of the latent virus in order to elevate Tax to its oncogenic threshold. We have previously found that DNA damaging agents, which usually induce apoptosis, can also activate the viral LTR an... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5281259 Sat, 01 Oct 2011 04:00:00 +0100 5281259 http://www.medworm.com/index.php?rid=5247213&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21926473%26dopt%3DAbstract Authors: Erkizan HV, Scher LJ, Gamble SE, Barber-Rotenberg JS, Sajwan KP, Uren A, Toretsky JA Abstract Ewing tumor is driven by the oncogenic EWS-FLI1 fusion protein that functions as an aberrant transcription factor. The identification of EWS-FLI1 protein partners is essential to enhance its vulnerability as a therapeutic target. We utilized phage display library screening against recombinant EWS-FLI1 protein. We identified 27 unique Ewing sarcoma binding peptides. The cytotoxicity evaluation of these peptides with in EWS-FLI1 containing cell lines yielded one potent peptide called ESAP1 (TMRGKKKRTRAN). ESAP1 binds EWS-FLI1 with 0.202 micromolar affinity as measured in surface plasmon resonance. The minimal interaction region of ESAP1 is characterized and found that the lysine res... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5247213 Fri, 23 Sep 2011 18:54:43 +0100 5247213 http://www.medworm.com/index.php?rid=5247212&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21926474%26dopt%3DAbstract Authors: Yu XG, Lichterfeld M Abstract Comment on: Chen H, et al. J Clin Invest 2011; 121:1549-60. PMID: 21926474 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5247212 Fri, 23 Sep 2011 18:54:32 +0100 5247212 http://www.medworm.com/index.php?rid=5247211&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21926475%26dopt%3DAbstract Authors: Adamo A, Barrero MJ, Belmonte JC Abstract Comment on: Adamo A, et al. Nat Cell Biol 2011; 13:652-60. PMID: 21926475 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5247211 Fri, 23 Sep 2011 18:54:21 +0100 5247211 http://www.medworm.com/index.php?rid=5247210&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21926476%26dopt%3DAbstract Authors: Bai Y, Zhou Z, Feng H, Zhou BR Abstract Comment on: Zhou et al. Nature 2011; 47:234-237, Hu et al. Genes Dev 2011; 25:901-6 and Cho et al. Proc Natl Acad Sci USA 2011; 108:9367-71. PMID: 21926476 [PubMed - as supplied by publisher] (Source: Cell Cycle) Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5247210 Fri, 23 Sep 2011 18:54:10 +0100 5247210 http://www.medworm.com/index.php?rid=5247209&cid=s_37760_171_f&fid=37760&url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21926477%26dopt%3DAbstract Authors: Lu WT, Lemonidis K, Drayton RM, Nouspikel T Abstract The Fanconi anaemia (FA) pathway is a DNA-damage inducible pathway critical for genomic stability. FA patients typically display high cancer susceptibility and hypersensitivity to DNA-damaging agents such as cross-linkers and ionizing radiation. A key step in the activation of the FA pathway is monoubiquitination of the FancD2 protein. Here we report that the FA pathway is downregulated by two distinct mechanisms upon differentiation of THP-1 and HL-60 leukaemia cells into macrophages. Firstly, qRT-PCR analysis revealed a transcriptional downregulation of most components of the FA complex, including FancD2. Secondly, DNA damage-induced monoubiquitination of the remaining FancD2 became deficient at various stages of diffe... Cell Cycle journals http://www.medworm.com/rss/comments.php?id=5247209 Fri, 23 Sep 2011 18:53:59 +0100 5247209