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        <title>Journal of Molecular Signaling via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Journal of Molecular Signaling' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Journal+of+Molecular+Signaling&t=Journal+of+Molecular+Signaling&s=Search&f=source]]></link>
        <lastBuildDate>Thu, 09 Feb 2012 16:56:47 +0100</lastBuildDate>
        <item>
            <title>The Caenorhabditis elegans D2-like dopamine receptor DOP-2 physically interacts with GPA-14, a G-alpha-i subunit</title>
            <link>http://www.medworm.com/index.php?rid=5635464&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F7%2F1%2F3</link>
            <description>Dopaminergic inputs are sensed on the cell surface by the seven-transmembrane dopamine receptors that belong to a superfamily of G-protein-coupled receptors (GPCRs). Dopamine receptors are classified as D1-like or D2-like receptors based on their homology and pharmacological profiles. In addition to well established G-protein coupled mechanism of dopamine receptors in mammalian system they can also interact with other signaling pathways. In C. elegans four dopamine receptors (dop-1, dop-2, dop-3 and dop-4) have been reported and they have been implicated in a wide array of behavioral and physiological processes. We performed this study to assign the signaling pathway for DOP-2, a D2-like dopamine receptor using a split-ubiquitin based yeast two-hybrid screening of a C. elegans cDNA library...</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5635464</comments>
            <pubDate>Thu, 26 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5635464</guid>        </item>
        <item>
            <title>Brain-derived neurotrophic factor receptor TrkB exists as a preformed dimer in living cells</title>
            <link>http://www.medworm.com/index.php?rid=5624812&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F7%2F1%2F2</link>
            <description>Conclusions:
Most, if not all, of the TrkB receptor has a preformed, yet inactive, homodimeric structure before BDNF binding. The intracellular domain of TrkB plays a crucial role in the spontaneous dimerization of the newly synthesized receptors, which occurs in ER. These findings provide new insight into an understanding of a molecular mechanism underlying transmembrane signaling mediated by NT receptors. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624812</comments>
            <pubDate>Tue, 24 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624812</guid>        </item>
        <item>
            <title>The adaptor protein p62/SQSTM1 in osteoclast signaling pathways</title>
            <link>http://www.medworm.com/index.php?rid=5568908&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F7%2F1%2F1</link>
            <description>Paget's disease of bone (PDB) is a skeletal disorder characterized by focal and disorganized increases in bone turnover and overactive osteoclasts. The discovery of mutations in the SQSTM1/p62 gene in numerous patients has identified protein p62 as an important modulator of bone turnover. In both precursors and mature osteoclasts, the interaction between receptor activator of NF-kappaB ligand (RANKL) and its receptor RANK results in signaling cascades that ultimately activate transcription factors, particularly NF-kappaB and NFATc1, promoting and regulating the osteoclast differentiation, activity, and survival. As a scaffold with multiple protein-protein interaction motifs, p62 is involved in virtually all the RANKL-activated osteoclast signaling pathways, along with being implicated in n...</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568908</comments>
            <pubDate>Wed, 04 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568908</guid>        </item>
        <item>
            <title>Canonical Wnt signaling is involved in switching from cell proliferation to myogenic differentiation of mouse myoblast cells</title>
            <link>http://www.medworm.com/index.php?rid=5292957&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F6%2F1%2F12</link>
            <description>Conclusions:
These results suggest that various Wnt ligands control subcellular beta-catenin localization, which regulate myoblast proliferation and myotube formation. Wnt signaling via beta-catenin likely acts as a molecular switch that regulates the transition from cell proliferation to myogenic differentiation. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5292957</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5292957</guid>        </item>
        <item>
            <title>E4BP4 facilitates glucocorticoid-evoked apoptosis of human leukemic CEM cells via upregulation of Bim</title>
            <link>http://www.medworm.com/index.php?rid=5292956&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F6%2F1%2F13</link>
            <description>Conclusion: Data presented here suggest that GC-mediated upregulation of E4BP4 facilitates Bim upregulation and apoptosis of CEM cells. Since the Bim promoter does not contain any consensus GRE or EBPRE sequences, induction of Bim may be a secondary response. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5292956</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5292956</guid>        </item>
        <item>
            <title>Characterization of the Rac guanine nucleotide exchange factor P-Rex1 in platelets</title>
            <link>http://www.medworm.com/index.php?rid=5191223&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F6%2F1%2F11</link>
            <description>Conclusions: These findings suggest that P-Rex1 is not required for Rac1-mediated platelet activation and that the GEF activities of P-Rex1 may be more specific to GPCR chemokine receptor mediated processes in immune cells and tumor cells. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5191223</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5191223</guid>        </item>
        <item>
            <title>G-patch domain and KOW motifs-containing protein, GPKOW; a nuclear RNA-binding protein regulated by protein kinase A</title>
            <link>http://www.medworm.com/index.php?rid=5191224&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F6%2F1%2F10</link>
            <description>ConclusionGPKOW is a RNA-binding protein that binds RNA in a PKA regulated fashion. Together with our previous results demonstrating that PKA regulates pre-mRNA splicing, our results suggest that PKA-phosphorylation is involved in regulating RNA processing at several steps. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5191224</comments>
            <pubDate>Tue, 30 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5191224</guid>        </item>
        <item>
            <title>Heterodimerization of beta2 Adrenergic Receptor and Somatostatin Receptor 5: Implications in Modulation of Signaling Pathway</title>
            <link>http://www.medworm.com/index.php?rid=5124421&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F6%2F1%2F9</link>
            <description>${item.shortDescription} (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5124421</comments>
            <pubDate>Thu, 11 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5124421</guid>        </item>
        <item>
            <title>AKAP12 and AKAP5 form higher-order hetero-oligomers</title>
            <link>http://www.medworm.com/index.php?rid=5117132&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F6%2F1%2F8</link>
            <description>${item.shortDescription} (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5117132</comments>
            <pubDate>Tue, 09 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5117132</guid>        </item>
        <item>
            <title>Combination of dasatinib and curcumin eliminates chemo-resistant colon cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5048330&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F6%2F1%2F7</link>
            <description>${item.shortDescription} (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5048330</comments>
            <pubDate>Tue, 19 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5048330</guid>        </item>
        <item>
            <title>Rad6B acts downstream of Wnt signaling to stabilize beta-catenin: Implications for a novel Wnt/beta-catenin target</title>
            <link>http://www.medworm.com/index.php?rid=5048331&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F6%2F1%2F6</link>
            <description>${item.shortDescription} (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5048331</comments>
            <pubDate>Sun, 17 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5048331</guid>        </item>
        <item>
            <title>Distinct roles of MK2 and MK5 in cAMP/PKA- and stress/p38MAPK-induced heat shock protein 27 phosphorylation</title>
            <link>http://www.medworm.com/index.php?rid=4827629&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F6%2F1%2F4</link>
            <description>Conclusion:
Our results suggest that in HEK293 cells MK2 is the HSP27 kinase engaged in stress-induced, but not cAMP-induced phosphorylation of HSP27, while MK5 seems to be the sole MK to mediate HSP27 phosphorylation in response to stimulation of the PKA pathway. Thus, despite the same substrate specificity towards HSP27, MK2 and MK5 are implicated in different signaling pathways causing actin reorganization. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4827629</comments>
            <pubDate>Sun, 15 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4827629</guid>        </item>
        <item>
            <title>AKAP5 and AKAP12 form homo-oligomers</title>
            <link>http://www.medworm.com/index.php?rid=4801622&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F6%2F1%2F3</link>
            <description>Conclusion:
Both AKAP5 and AKAP12 display the capacity to form supermolecular homo-oligomeric structures that likely influence the localization and function of these molecular scaffolds. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4801622</comments>
            <pubDate>Sun, 08 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4801622</guid>        </item>
        <item>
            <title>Activation of K-RAS by co-mutation of codons 19 and 20 is transforming</title>
            <link>http://www.medworm.com/index.php?rid=4544424&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F6%2F1%2F2</link>
            <description>The K-RAS oncogene is widely mutated in human cancers. Activating mutations in K-RAS give rise to constitutive signalling through the MAPK/ERK and PI3K/AKT pathways promoting increased cell division, altered apoptosis and transformation. The majority of activating mutations in K-RAS are located in codons 12 and 13. In a colorectal cancer we identified a novel K-RAS co-mutation that altered codons 19 and 20 resulting in transitions at both codons (L19F/T20A) in the same allele. Using focus forming transformation assays in vitro , we showed that co-mutation of L19F/T20A in K-RAS demonstrated intermediate transforming ability that was greater than that of individual L19F and T20A mutants, but less than that of G12D and G12V K-RAS mutants. This demonstrated the synergistic effects of co-mutati...</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4544424</comments>
            <pubDate>Thu, 03 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4544424</guid>        </item>
        <item>
            <title>Probing the physical nature and composition of signalsomes</title>
            <link>http://www.medworm.com/index.php?rid=4337085&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F6%2F1%2F1</link>
            <description>Conclusion: Dvl3-based punctae/signalsomes made visible by fluorescent microscopy now can be interrogated by advanced physical means, defining such properties as signalsome Mr/MW, molecular composition, and intracellular locale. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4337085</comments>
            <pubDate>Tue, 11 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4337085</guid>        </item>
        <item>
            <title>Peroxisome proliferator-activated receptor gamma ligand-mediated apoptosis of hepatocellular carcinoma cells depends upon modulation of PI3Kinase pathway independent of Akt</title>
            <link>http://www.medworm.com/index.php?rid=4257995&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F5%2F1%2F20</link>
            <description>Conclusion:
These studies indicate that TRG-induced apoptosis is modulated by PI3K pathway in a novel Akt-independent manner, which might contribute to its tumor promoting effects. Since PI3K activation is linked with various cancers, combination therapy utilizing TRG and PI3K inhibitors has the potential to not only increase the efficacy of TRG as a chemotherapeutic agent but also reduce its off target effects. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4257995</comments>
            <pubDate>Mon, 13 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4257995</guid>        </item>
        <item>
            <title>Dishevelled-3 C-terminal His single amino acid repeats are obligate for Wnt5a activation of non-canonical signaling</title>
            <link>http://www.medworm.com/index.php?rid=4196281&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F5%2F1%2F19</link>
            <description>Conclusions:
The C-terminal third of Dvl3 and His single amino acid repeats 637,638 and 647,648 (which are unique to and conserved in Dvl3) are essential for Wnt5a activation of the non-canonical pathway, but not for the Wnt3a activation of the canonical pathway. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4196281</comments>
            <pubDate>Tue, 23 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4196281</guid>        </item>
        <item>
            <title>TLN-4601 suppresses growth and induces apoptosis of pancreatic carcinoma cells through inhibition of Ras-ERK MAPK signaling</title>
            <link>http://www.medworm.com/index.php?rid=4132531&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F5%2F1%2F18</link>
            <description>Conclusion:
These data, together with phase I/II clinical data showing tolerability of TLN-4601, support conducting a clinical trial in advanced pancreatic cancer patients. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4132531</comments>
            <pubDate>Tue, 02 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4132531</guid>        </item>
        <item>
            <title>The adaptor protein SH2B1beta reduces hydrogen peroxide-induced cell death in PC12 cells and hippocampal neurons</title>
            <link>http://www.medworm.com/index.php?rid=4011563&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F5%2F1%2F17</link>
            <description>Conclusions:
Overexpressing the adaptor protein SH2B1beta enhanced H2O2-induced PI3K-AKT and MEK-ERK1/2 signaling, reduced nucleus-localized FoxOs and the expression of a pro-apoptotic gene, FasL. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4011563</comments>
            <pubDate>Sun, 26 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4011563</guid>        </item>
        <item>
            <title>Chaperones contribute to G protein coupled receptor oligomerization, but do not participate in assembly of the G protein with the receptor signaling complex</title>
            <link>http://www.medworm.com/index.php?rid=3998005&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F5%2F1%2F16</link>
            <description>Conclusions:
Overall, our results suggest that variations among receptor oligomers occur early in the synthesis/maturation processes, and that chaperones will interact more specifically with some receptor pairs than others to allow the formation of certain receptor pairs, while others will contribute to the folding and maturation of receptors without any effect on receptor assembly within a signaling complex. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3998005</comments>
            <pubDate>Thu, 23 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3998005</guid>        </item>
        <item>
            <title>AMPK-induced activation of Akt by AICAR is mediated by IGF-1R dependent and independent mechanisms in acute lymphoblastic leukemia</title>
            <link>http://www.medworm.com/index.php?rid=3998006&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F5%2F1%2F15</link>
            <description>Conclusions:
Our study demonstrates that AMPK activates Akt through IGF-1R dependent and independent mechanisms. Co-targeting IGF-1R and related downstream metabolic and oncogenic signaling pathways represent a potential strategy for future translation into novel ALL therapies. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3998006</comments>
            <pubDate>Wed, 22 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3998006</guid>        </item>
        <item>
            <title>The dietary bioflavonoid quercetin synergizes with epigallocathechin gallate (EGCG) to inhibit prostate cancer stem cell characteristics, invasion, migration and epithelial-mesenchymal transition.</title>
            <link>http://www.medworm.com/index.php?rid=3880284&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F5%2F1%2F14</link>
            <description>Conclusion:
Since carcinogenesis is a complex process, combination of bioactive dietary agents with complementary activities will be beneficial for prostate cancer prevention and/or treatment. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3880284</comments>
            <pubDate>Tue, 17 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3880284</guid>        </item>
        <item>
            <title>Novel cis-trans interactions are involved in post-transcriptional regulation of cyclin-dependent kinase inhibitor p21WAF1/CIP1 mRNA.</title>
            <link>http://www.medworm.com/index.php?rid=3861425&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F5%2F1%2F12</link>
            <description>Conclusion:
CD437 regulates cell growth in part by regulating stability of p21WAF1/CIP1 mRNA that involves specific RNA-protein interactions that are phosphorylation-dependent, while not requiring nascent transcription or protein synthesis. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3861425</comments>
            <pubDate>Wed, 11 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3861425</guid>        </item>
        <item>
            <title>Transformation by a nucleotide-activated P2Y receptor is mediated by activation of Galphai, Galphaq and Rho-dependent signaling pathways</title>
            <link>http://www.medworm.com/index.php?rid=3783763&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F5%2F1%2F11</link>
            <description>Conclusions:
Our data suggest that coordinated activation of Galphaq and Galphai may link the tP2YR and possibility the Mas oncogene with signaling pathways resulting in activation of Rho family proteins to promote cellular transformation. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3783763</comments>
            <pubDate>Thu, 22 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3783763</guid>        </item>
        <item>
            <title>Inhibition of PI3K/AKT and MAPK/ERK pathways causes activation of FOXO transcription factor, leading to cell cycle arrest and apoptosis in pancreatic cancer</title>
            <link>http://www.medworm.com/index.php?rid=3766754&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F5%2F1%2F10</link>
            <description>Conclusion:
These data suggest that inhibition of PI3K/AKT and ERK pathways activated FOXO transcription factors and enhanced SFN-induced FOXO transcriptional activity, leading to cell cycle arrest and apoptosis in pancreatic cancer cells. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3766754</comments>
            <pubDate>Sun, 18 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3766754</guid>        </item>
        <item>
            <title>EGFR/Met association regulates EGFR TKI resistance in breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=3746353&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F5%2F1%2F8</link>
            <description>Breast cancers show a lack of response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), despite 30% of tumors expressing EGFR. The mechanism of this resistance is unknown; however, we have recently shown that Met kinase activity compensates for loss of EGFR kinase activity in cell culture models. Met has been implicated in the pathogenesis of breast tumors and therefore may cooperate with EGFR for tumor growth. Here we have found that EGFR phosphorylation and cell proliferation is in part regulated by Met expression.  In addition, we found that Met constitutive phosphorylation occurred independent of the Met ligand hepatocyte growth factor (HGF). Ligand-independent Met phosphorylation is mediated by Met amplification, mutation, or overexpression and by Met inte...</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3746353</comments>
            <pubDate>Sun, 11 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3746353</guid>        </item>
        <item>
            <title>A novel mechanism of cell growth regulation by cell cycle and apoptosis regulatory protein (CARP)-1.</title>
            <link>http://www.medworm.com/index.php?rid=3717954&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F5%2F1%2F7</link>
            <description>Conclusion:
CARP-1 threonine667 regulates H89-dependent signaling by a novel pathway that involves modulation of CARP-1 interaction with TAZ and transcriptional down-regulation of c-myc. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3717954</comments>
            <pubDate>Wed, 30 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3717954</guid>        </item>
        <item>
            <title>Adenoviral oncoprotein E1B55K mediates colocalization of SSBP2 and PML in response to stress</title>
            <link>http://www.medworm.com/index.php?rid=3655285&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F5%2F1%2F6</link>
            <description>Transient expression of adenoviral oncoprotein E1B55K in normal cells induces aggresome formation and sequestration of critical host proteins in aggresomes. Our previous studies reported that Sequence Specific Binding Protein 2 (SSBP2), a candidate tumor suppressor is recruited to aggresomes in adenovirally transformed human embryonal kidney 293 (HEK293) cells[1].  To understand the extent and significance of the E1B55K-SSBP2 interactions in these cells, we have examined SSBP2 localization under conditions of stress in HEK293 cells.  SSBP2 localizes to PML- Nuclear Bodies (PML-NBs) in response to inhibition of nuclear export, treatment with etoposide, hydroxyurea or gamma irradiation only in HEK293 cells. Furthermore, the PML-NBs grow in size and number in response to radiation over a 24 h...</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3655285</comments>
            <pubDate>Thu, 10 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3655285</guid>        </item>
        <item>
            <title>Zinc release from thapsigargin/IP3-sensitive stores in cultured cortical neurons</title>
            <link>http://www.medworm.com/index.php?rid=3602982&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F5%2F1%2F5</link>
            <description>Conclusions:
Taken together, these results suggest that Zn2+ is sequestered into thapsigargin/IP3-sensitive stores and is released upon agonist stimulation. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3602982</comments>
            <pubDate>Tue, 25 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3602982</guid>        </item>
        <item>
            <title>NSC109268 potentiates cisplatin-induced cell death in a p53-independent manner</title>
            <link>http://www.medworm.com/index.php?rid=3548818&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F5%2F1%2F4</link>
            <description>Conclusions:
These results demonstrate that NSC109268 enhances sensitivity of ovarian cancer 2008 cells to cisplatin independent of p53. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3548818</comments>
            <pubDate>Sun, 09 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3548818</guid>        </item>
        <item>
            <title>AKAR2-AKAP12 fusion protein &quot;biosenses&quot; dynamic phosphorylation and localization of a GPCR-based scaffold</title>
            <link>http://www.medworm.com/index.php?rid=3493765&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F5%2F1%2F3</link>
            <description>Conclusion:
The dynamic phosphorylation of AKAP12 &quot;biosensed&quot; by AKAR2-AKAP12 reveals the scaffold in association with the cell membrane, undergoing rapid phosphorylation by PKA. The perinuclear, cytoplasmic accumulation of phosphorylated scaffold reflects the phosphorylated, PKA-activated form of AKAP12, which catalyzes the resensitization and recycling of desensitized, internalized G-protein-coupled receptors. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3493765</comments>
            <pubDate>Wed, 21 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3493765</guid>        </item>
        <item>
            <title>Genetic and functional characterization of putative Ras/Raf interaction inhibitors in C. elegans and mammalian cells</title>
            <link>http://www.medworm.com/index.php?rid=3297846&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F5%2F1%2F2</link>
            <description>Conclusions:
We have effectively utilized C. elegans as an in vivo genetic system to evaluate the activity and selectivity of inhibitors intended to target the Ras-Raf-MAPK pathway. We demonstrated the ability of MCP110 to disrupt, at the level of Ras/Raf, the Muv phenotype induced by chronic activation of this pathway in C. elegans. In mammalian cells, we not only demonstrated MCP-mediated blockade of the physical interaction between Ras and Raf, but also narrowed the site of interaction on Raf to the RBD, and showed consequent functional impairment of the Ras-Raf-MEK-ERK pathway in both in vivo and cell-based systems. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3297846</comments>
            <pubDate>Tue, 23 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3297846</guid>        </item>
        <item>
            <title>AMPK exerts dual regulatory effects on the PI3K pathway</title>
            <link>http://www.medworm.com/index.php?rid=3287230&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F5%2F1%2F1</link>
            <description>Conclusion	Our present study demonstrates that AMPK exerts dual effects on the PI3K pathway, stimulating PI3K/Akt and inhibiting mTOR/S6K. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3287230</comments>
            <pubDate>Thu, 18 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3287230</guid>        </item>
        <item>
            <title>Molecular mechanism of regulation of OGG1: tuberin deficiency results in cytoplasmic redistribution of transcriptional factor NF-YA</title>
            <link>http://www.medworm.com/index.php?rid=3128757&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F4%2F1%2F8</link>
            <description>The tuberous sclerosis complex (TSC) is caused by defects in one of two tumor suppressor genes, TSC-1 or TSC-2. TSC-2 gene encodes tuberin, a protein involved in the pathogenesis of kidney tumors, both angiomyolipomas and renal cell carcinomas. On the other hand, mice-deficient in the DNA repair enzyme OGG1 spontaneously develop adenoma and carcinoma. Downregulation of tuberin results in a marked decrease of OGG1 and accumulation of oxidative DNA damage, (8-oxodG) in cultured cells. In addition, tuberin haploinsufficiency is associated with the loss of OGG1 and accumulation of 8-oxodG in rat kidney tumor. Deficiency in tuberin results in decreased OGG1 and NF-YA protein expression and increased 8-oxodG in kidney tumor from TSC patients. In the current study, molecular mechanisms by which t...</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3128757</comments>
            <pubDate>Tue, 29 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3128757</guid>        </item>
        <item>
            <title>Immature and mature species of the human Prostacyclin Receptor are ubiquitinated and targeted to the 26S proteasomal or lysosomal degradation pathways, respectively</title>
            <link>http://www.medworm.com/index.php?rid=2831565&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F4%2F1%2F7</link>
            <description>Conclusion:
These findings indicate that the hIP is post-translationally modified by ubiquitination, which targets the immature species to the 26S proteasomal degradation pathway and the mature species to the lysosomal degradation pathway. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2831565</comments>
            <pubDate>Thu, 24 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2831565</guid>        </item>
        <item>
            <title>Overexpression of tissue inhibitors of metalloproteinase 2 up-regulates NF-kappaB activity in melanoma cells</title>
            <link>http://www.medworm.com/index.php?rid=2633793&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F4%2F1%2F4</link>
            <description>Conclusion: Our data demonstrate that the expression level of TIMP-2 protein can directly modulate the NF-kappaB pathway in human melanoma cells. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2633793</comments>
            <pubDate>Wed, 22 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2633793</guid>        </item>
        <item>
            <title>Expression analyses of nuclear receptor genes in breast cancer cell lines exposed to soy phytoestrogens after BRCA2 knockdown by TaqMan Low-Density Array (TLDA)</title>
            <link>http://www.medworm.com/index.php?rid=2413376&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F4%2F1%2F3</link>
            <description>Conclusions:
Our results seemed to implicate the oncosuppressor BRCA2 and the phytoestrogen pathways in different nuclear gene expressions via an ER-independent manner. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2413376</comments>
            <pubDate>Thu, 14 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2413376</guid>        </item>
        <item>
            <title>Membrane estrogen receptor-α-mediated nongenomic actions of phytoestrogens in GH3/B6/F10 pituitary tumor cells</title>
            <link>http://www.medworm.com/index.php?rid=2402584&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F4%2F1%2F2</link>
            <description>Conclusion:
Phytoestrogens were much more potent in mediating these nongenomic responses (activation of MAPKs, PRL release, and increased intracellular [Ca2+]) via mERα than was previously reported for genomic responses. The unique non-monotonic dose responses and variant signaling patterns caused by E2 and all tested phytoestrogens suggest that complex and multiple signaling pathways or binding partners could be involved. By activating these different nongenomic signaling pathways, phytoestrogens could have significant physiological consequences for pituitary cell functions. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2402584</comments>
            <pubDate>Tue, 28 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2402584</guid>        </item>
        <item>
            <title>AKT/eNOS signaling module functions as a potential feedback loop in the growth hormone signaling pathway</title>
            <link>http://www.medworm.com/index.php?rid=2295773&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F4%2F1%2F1</link>
            <description>Conclusions:
The MAP kinase and CDC2 kinase-dependent intracellular mechanisms are involved in or are the targets of the GH's action processes, and these activities are probably directly or indirectly modulated by AKT/PKB pathways. We propose that the AKT/PKB-eNOS module likely functions as a negative feedback mediator of GH actions. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2295773</comments>
            <pubDate>Wed, 25 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2295773</guid>        </item>
        <item>
            <title>Differential role of beta-arrestin ubiquitination in agonist-promoted down-regulation of M1 vs M2 muscarinic acetylcholine receptors</title>
            <link>http://www.medworm.com/index.php?rid=2222043&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F3%2F1%2F20</link>
            <description>Conclusion:
These findings indicate that ubiquitination of β-arrestin has a distinct role in the differential trafficking and degradation of M1 and M2 mAChRs. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2222043</comments>
            <pubDate>Wed, 03 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2222043</guid>        </item>
        <item>
            <title>Differential role of beta-arrestin ubiquitination in agonist-promoted down-regulation of M1 vs M2 muscarinic acetylcholine receptors.</title>
            <link>http://www.medworm.com/index.php?rid=2010777&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F3%2F1%2F20</link>
            <description>Conclusions:
These findings indicate that ubiquitination of beta-arrestin has a distinct role in the differential trafficking and degradation of M1 and M2 mAChRs. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2010777</comments>
            <pubDate>Wed, 03 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2010777</guid>        </item>
        <item>
            <title>Cell cycle arrest in metformin treated breast cancer cells involves activation of AMPK, downregulation of cyclin D1, and  requires  p27Kip1 or p21Cip1</title>
            <link>http://www.medworm.com/index.php?rid=2004796&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F3%2F1%2F18</link>
            <description>Conclusions: Cell cycle arrest in response to metformin requires CDK inhibitors in addition to AMPK activation and cyclin D1 downregulation. This is of interest because many cancers are associated with loss or downregulation of CDK inhibitors and the results may be relevant to the development of anti-tumor reagents that target the AMPK pathway (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2004796</comments>
            <pubDate>Mon, 01 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2004796</guid>        </item>
        <item>
            <title>SFRP-4 abrogates Wnt-3a-induced β-catenin and Akt/PKB signalling and reverses a Wnt-3a-imposed inhibition of in vitro mammary differentiation</title>
            <link>http://www.medworm.com/index.php?rid=1494134&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F3%2F1%2F10</link>
            <description>Conclusion:
This study demonstrates that Wnt-3a treatment activates the Wnt signalling pathway and interferes with in vitro differentiation of mammary co-cultures to β-casein production in response to lactogenic hormones. Similarly, in another measure of differentiation, following Wnt-3a treatment mammary epithelial cells could be shown to up-regulate the cyclin D1 and connexin-43 genes while phenotypically they show increased transepithelial resistance across the cell monolayer. All these behavioural changes can be blocked in mammary epithelial cells expressing SFRP-4. Thus, our data illustrate in an in vitro model a mechanism by which SFRP-4 can modulate a differentiation response to Wnt-3a. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1494134</comments>
            <pubDate>Fri, 02 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1494134</guid>        </item>
        <item>
            <title>Enhanced catharanthine and vindoline production in suspension cultures of Catharanthus roseus by ultraviolet-B light</title>
            <link>http://www.medworm.com/index.php?rid=1399011&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F3%2F1%2F9</link>
            <description>Suspension cultures of Catharanthus roseus were used to evaluate ultraviolet-B (UV-B) treatment as an abiotic elicitor of secondary metabolites. A dispersed cell suspension culture from C. roseus leaves in late exponential phase and stationary phase were irradiated with UV-B for 5 min. The stationary phase cultures were more responsive to UV-B irradiation than late exponential phase cultures. Catharanthine and vindoline increased 3-fold and 12-fold, respectively on treatment with a 5-min UV-B irradiation. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1399011</comments>
            <pubDate>Fri, 25 Apr 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1399011</guid>        </item>
        <item>
            <title>Src homology 2 (SH2) domain containing protein tyrosine phosphatase-1 (SHP-1) dephosphorylates VEGF Receptor-2 and attenuates endothelial DNA synthesis, but not migration</title>
            <link>http://www.medworm.com/index.php?rid=1340077&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F3%2F1%2F8</link>
            <description>Conclusions:
Taken together our results define the tyrosine residues of KDR that are regulated by SHP-1 and also elucidates a novel feed back loop where SHP-1 is activated upon VEGF treatment through c-Src and controls KDR induced DNA synthesis, eventually leading to controlled angiogenesis. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1340077</comments>
            <pubDate>Mon, 31 Mar 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1340077</guid>        </item>
        <item>
            <title>Inhibition of PI3K/AKT and MEK/ERK pathways act synergistically to enhance antiangiogenic effects of EGCG through activation of FOXO transcription factor</title>
            <link>http://www.medworm.com/index.php?rid=1316529&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F3%2F1%2F7</link>
            <description>Conclusion:
Inhibition of PI3K/AKT and MEK/ERK pathways act synergistically to regulate antiangiogenic effects of EGCG through activation of FOXO transcription factors. The activation of FOXO transcription factors through inhibition of these two pathways may have physiological significance in management of diabetic retinopathy, rheumatoid arthritis, psoriasis, cardiovascular diseases, and cancer. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1316529</comments>
            <pubDate>Thu, 20 Mar 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1316529</guid>        </item>
        <item>
            <title>The alpha1D-adrenergic receptor is expressed intracellularly and coupled to increases in intracellular calcium and reactive oxygen species in human aortic smooth muscle cells</title>
            <link>http://www.medworm.com/index.php?rid=1261451&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F3%2F1%2F6</link>
            <description>Conclusions:
Our results suggest that the dimerization of the alpha-1D-AR with other ARs does not alter the cellular expression or functional response characteristics of the alpha-1D-AR. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1261451</comments>
            <pubDate>Wed, 27 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1261451</guid>        </item>
        <item>
            <title>Binding mode prediction of conformationally restricted anandamide analogs within the CB1 receptor</title>
            <link>http://www.medworm.com/index.php?rid=1259740&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F3%2F1%2F5</link>
            <description>Conclusions:
Analyses of multiple poses of conformationally-restricted anandamide analogs permitted identification of favored amino acid interactions within the CB1 receptor binding pocket. A ligand possessing both high affinity and cannabinoid agonist efficacy was able to interact with both polar and hydrophobic interaction sites utilized by the potent and efficacious non-classical cannabinoid CP55940. In contrast, other analogs characterized by reduced affinity or efficacy exhibited less favorable interactions with those key residues. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1259740</comments>
            <pubDate>Tue, 26 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1259740</guid>        </item>
        <item>
            <title>Dramatic inhibition of osteoclast sealing ring formation and bone resorption in vitro by a WASP-peptide containing pTyr294 amino acid</title>
            <link>http://www.medworm.com/index.php?rid=1244878&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F3%2F1%2F4</link>
            <description>Wiskott Aldrich Syndrome protein (WASP) has a unique regulatory role in sealing ring formation and bone resorption in osteoclasts. Here, using the TAT-transduction method, we show the possible role of WASP domain(s) in sealing ring formation and bone resorption. Transduction of TAT-fused full-length WASP peptide induced Arp2/3 complex formation, F-actin content, sealing ring formation and bone resorption. Transduction of WASP peptides containing basic, verpolin-central, pTyr294, and proline-rich regions inhibited the processes listed above at various levels. The ability to resorb bone by WASP peptides containing basic, verpolin-central, and proline-rich regions was reduced and the resorbed area matched the size of the sealing ring. However, osteoclasts transduced with WASP peptide containi...</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1244878</comments>
            <pubDate>Wed, 20 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1244878</guid>        </item>
        <item>
            <title>Retinoic Acid decreases ATF-2 phosphorylation and sensitizes melanoma cells to taxol-mediated growth inhibition</title>
            <link>http://www.medworm.com/index.php?rid=1224958&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F3%2F1%2F3</link>
            <description>Cutaneous melanoma is often resistant to chemo- and radiotherapy. This resistance has recently been demonstrated to be due, at least in part, to high activating transcription factor 2 (ATF 2) activity in these tumors. In concordance with these reports, we found that B16 mouse melanoma cells had higher levels of ATF-2 than immortalized, but non-malignant mouse melanocytes. In addition, the melanoma cells had a much higher amount of phosphorylated (active) ATF-2 than the immortalized melanocytes. In the course of determining how retinoic acid (RA) stimulates activating protein-1 (AP-1) activity in B16 melanoma, we discovered that this retinoid decreased the phosphorylation of ATF-2. It appears that this effect is mediated through p38 MAPK, because RA decreased p38 phosphorylation (activation...</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1224958</comments>
            <pubDate>Tue, 12 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1224958</guid>        </item>
        <item>
            <title>Scaffolding proteins in G-protein signaling</title>
            <link>http://www.medworm.com/index.php?rid=991668&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F2%2F1%2F13</link>
            <description>Heterotrimeric G proteins are ubiquitous signaling partners of seven transmembrane-domain G-protein-coupled receptors (GPCRs), the largest (and most important pharmacologically) receptor family in mammals. A number of scaffolding proteins have been identified that regulate various facets of GPCR signaling. In this review, we summarize current knowledge concerning those scaffolding proteins that are known to directly bind heterotrimeric G proteins, and discuss the composition of the protein complexes they assemble and their effects on signal transduction. Emerging evidence about possible ways of regulation of activity of these scaffolding proteins is also discussed. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=991668</comments>
            <pubDate>Tue, 30 Oct 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">991668</guid>        </item>
        <item>
            <title>Abundance, complexation, and trafficking of Wnt/beta-catenin signaling elements in response to Wnt3</title>
            <link>http://www.medworm.com/index.php?rid=978901&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F2%2F1%2F11</link>
            <description>Conclusions:
This study provides a detailed biochemical analysis of signaling elements key to Wnt3a regulation of the canonical pathway. We quantify, for the first time, the Wnt-dependent regulation of cellular abundance and intracellular trafficking of these signaling molecules. In contrast, we observe little effect of Wnt3a stimulation on the level of protein-protein interactions among these constituents of Axin-based complexes themselves. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=978901</comments>
            <pubDate>Thu, 25 Oct 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">978901</guid>        </item>
        <item>
            <title>Phosphoprotein phosphatase-2A docks to Dishevelled and counterregulates Wnt3a/beta-catenin signaling</title>
            <link>http://www.medworm.com/index.php?rid=978900&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F2%2F1%2F12</link>
            <description>Conclusions:
In current study, we showed new roles of phosphoprotein phosphatase-2A in Wnt/beta-catenin signaling pathway: effect on protein expression, effect on protein trafficking, retention of molecules in subcellular compartments, and regulation of enzymatic activity of several key players. Docking of phosphoprotein phosphatase-2A by Dishevelled-2 suppresses phosphatase activity and explains in part the central role of this phosphatase in the counterregulation of the Wnt/beta-catenin signaling pathway. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=978900</comments>
            <pubDate>Thu, 25 Oct 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">978900</guid>        </item>
        <item>
            <title>Curcumin enhances the apoptosis-inducing potential of TRAIL in prostate cancer cells: molecular mechanisms of apoptosis, migration and angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=927636&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F2%2F1%2F10</link>
            <description>Conclusion:
The ability of curcumin to inhibit capillary tube formation and cell migration, and enhance the therapeutic potential of TRAIL suggests that curcumin alone or in combination with TRAIL can be used for prostate cancer prevention and/or therapy. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=927636</comments>
            <pubDate>Thu, 04 Oct 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">927636</guid>        </item>
        <item>
            <title>PI3 K/Akt/mTOR-mediated translational control regulates proliferation and differentiation of lineage-restricted RoSH stem cell lines</title>
            <link>http://www.medworm.com/index.php?rid=895449&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F2%2F1%2F9</link>
            <description>Conclusion:
This study highlights translation regulation as a critical regulatory mechanism during proliferation and differentiation in stem cells. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=895449</comments>
            <pubDate>Tue, 25 Sep 2007 00:29:06 +0100</pubDate>
            <guid isPermaLink="false">895449</guid>        </item>
        <item>
            <title>Ligand-dependent localization and intracellular stability of sigma-1 receptors in CHO-K1 cells.</title>
            <link>http://www.medworm.com/index.php?rid=887954&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F2%2F1%2F8</link>
            <description>Conclusions:
Ligand activated sigma-1 receptors translocate into FAC from a pool of receptors stored in ER lipid rafts presumably for inhibition of Kv1.4 channels. Stabilization of actin filaments is likely to be important for targeting sigma-1 receptors to Focal Adhesion Contacts in CHO-K1 cells. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=887954</comments>
            <pubDate>Thu, 20 Sep 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">887954</guid>        </item>
        <item>
            <title>Clusterin expression can be modulated by changes in TCF1-mediated Wnt signaling</title>
            <link>http://www.medworm.com/index.php?rid=736184&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F2%2F1%2F6</link>
            <description>Conclusion:
In conclusion, we have demonstrated that the Wnt signaling pathway specifically regulates one out of three CLU mRNA variants via TCF1. This CLU transcript is shorter at the 5' end than reported by the RefSeq database, and produces the intracellular 60 kDa CLU protein isoform which is secreted as a ~80 kDa protein after post-translational processing. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=736184</comments>
            <pubDate>Mon, 16 Jul 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">736184</guid>        </item>
        <item>
            <title>Role of RGM coreceptors in bone morphogenetic protein signaling</title>
            <link>http://www.medworm.com/index.php?rid=716325&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F2%2F1%2F4</link>
            <description>Conclusions:
Our results demonstrate that the RGMs play a significant role in BMP signaling and reveal that these molecules cannot functionally compensate for one another. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=716325</comments>
            <pubDate>Thu, 05 Jul 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">716325</guid>        </item>
        <item>
            <title>PNRC is a unique nuclear receptor coactivator that stimulates RNA polymerase III-dependent transcription</title>
            <link>http://www.medworm.com/index.php?rid=716324&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F2%2F1%2F5</link>
            <description>Conclusion:
Here, we demonstrate that human PNRC stimulates RNA pol III transcription through its interaction with the subunit RPC39 of RNA pol III.
PNRC is a unique coactivator that has profound effects on many aspects of cellular function by directly influencing both RNA pol II- and RNA pol III-dependent transcription. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=716324</comments>
            <pubDate>Thu, 05 Jul 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">716324</guid>        </item>
        <item>
            <title>Molecular mechanisms mediating the G protein-coupled receptor regulation of cell cycle progression</title>
            <link>http://www.medworm.com/index.php?rid=440483&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F2%2F1%2F2</link>
            <description>G protein-coupled receptors are key regulators of cellular communication, mediating the efficient coordination of a cell's responses to extracellular stimuli. When stimulated these receptors modulate the activity of a wide range of intracellular signalling pathways that facilitate the ordered development, growth and reproduction of the organism. There is now a growing body of evidence examining the mechanisms by which G protein-coupled receptors are able to regulate the expression, activity, localization and stability of cell cycle regulatory proteins that either promote or inhibit the initiation of DNA synthesis. In this review, we will detail the intracellular pathways that mediate the G protein-coupled receptor regulation of cellular proliferation, specifically the progression from the ...</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=440483</comments>
            <pubDate>Mon, 26 Feb 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">440483</guid>        </item>
        <item>
            <title>ArhGAP9, a novel MAP kinase docking protein, inhibits Erk and p38 activation through WW domain binding</title>
            <link>http://www.medworm.com/index.php?rid=400168&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F2%2F1%2F1</link>
            <description>We have identified human ArhGAP9 as a novel MAP kinase docking protein that interacts with Erk2 and p38alpha through complementarily charged residues in the WW domain of ArhGAP9 and the CD domains of Erk2 and p38alpha. This interaction sequesters the MAP kinases in their inactive states through displacement of MAP kinase kinases targeting the same sites. While over-expression of wild type ArhGAP9 caused MAP kinase activation by the epidermal growth factor receptor (EGFR) to be suppressed and preserved the actin stress fibres in quiescent Swiss 3T3 fibroblasts, over-expression of an ArhGAP9 mutant defective in MAP kinase binding restored EGFR-induced MAP kinase activation and resulted in significant disruption of the stress fibres, consistent with the role of Erk activation in disassembly o...</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=400168</comments>
            <pubDate>Tue, 06 Feb 2007 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">400168</guid>        </item>
        <item>
            <title>Rac inhibits thrombin-induced Rho activation: evidence of a Pak-dependent GTPase crosstalk</title>
            <link>http://www.medworm.com/index.php?rid=362779&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F1%2F1%2F8</link>
            <description>The strict spatio-temporal control of Rho GTPases is critical for many cellular functions, including cell motility, contractility, and growth. In this regard, the prototypical Rho family GTPases, Rho, Rac, and Cdc42 regulate the activity of each other by a still poorly understood mechanism. Indeed, we found that constitutively active forms of Rac inhibit stress fiber formation and Rho stimulation by thrombin. Surprisingly, a mutant of Rac that is unable to activate Pak1 failed to inhibit thrombin signaling to Rho. To explore the underlying mechanism, we investigated whether Pak1 could regulate guanine nucleotide exchange factors (GEFs) for Rho. We found that Pak1 associates with P115-RhoGEF but not with PDZ-RhoGEF or LARG, and knock down experiments revealed that P115-RhoGEF plays a major ...</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=362779</comments>
            <pubDate>Wed, 06 Dec 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">362779</guid>        </item>
        <item>
            <title>Estradiol effects on the dopamine transporter – protein levels, subcellular location, and function</title>
            <link>http://www.medworm.com/index.php?rid=362782&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F1%2F1%2F5</link>
            <description>Conclusion:
Our results suggest that physiological levels of E2 may act to sequester DAT in intracellular compartments where the transporter's second extramembrane loop is inaccessible (inside vesicles) and that rapid estrogenic actions on this differentiated neuronal cell type may be regulated via membrane ERs of several types. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=362782</comments>
            <pubDate>Tue, 05 Dec 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">362782</guid>        </item>
        <item>
            <title>Amino terminal tyrosine phosphorylation of human MIXL1</title>
            <link>http://www.medworm.com/index.php?rid=362781&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F1%2F1%2F6</link>
            <description>Seven members of the Mix family of paired-type homeoproteins regulate mesoderm/endoderm differentiation in amphibians. In mammals, the MIXL1 (Mix. 1 homeobox [Xenopus laevis]-like gene 1) gene is the sole representative of this family. Unlike the amphibian Mix genes that encode an open reading frame of &gt;300 amino acids, mammalian MIXL1 encodes a smaller protein (~230aa). However, mammalian MIXL1 contains a unique proline-rich domain (PRD) with a potential to interact with signal transducing Src homolgy 3 (SH3) domains. Notably, human MIXL1 also contains a unique tyrosine residue Tyr20 that is amino-terminal to the PRD. Here we report that mammalian MIXL1 protein is phosphorylated at Tyr20 and the phosphorylation is dramatically reduced in the absence of PRD. Our findings are consistent wit...</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=362781</comments>
            <pubDate>Tue, 05 Dec 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">362781</guid>        </item>
        <item>
            <title>Agonist mediated internalization of M2 mAChR is β-arrestin-dependent</title>
            <link>http://www.medworm.com/index.php?rid=362780&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F1%2F1%2F7</link>
            <description>Conclusion:
In summary, this study demonstrates that agonist-promoted internalization of M2 mAChRs is β-arrestin- and clathrin-dependent, and that the receptor stably co-localizes with β-arrestin in early endosomal vesicles. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=362780</comments>
            <pubDate>Tue, 05 Dec 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">362780</guid>        </item>
        <item>
            <title>An open access journal of molecular signaling: a critical need at a critical time</title>
            <link>http://www.medworm.com/index.php?rid=362784&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F1%2F1%2F1</link>
            <description>Molecular signaling is an exponentially growing field that encompasses different molecular aspects of cell signaling underlying normal and pathological conditions. This area also focuses on defining the genetic and epigenetic changes that modulate the signaling properties of cells and the resultant physiological as well as pathological conditions. Therefore, rapid publication of results from these endeavors and, more importantly, free access to such publications can truly accelerate the progress in this field leading to the development of novel targeted drugs. With this goal in mind, Journal of Molecular Signaling, a journal fully devoted to open access publishing of rigorously peer-reviewed quality manuscripts in the molecular signaling area of research, is being launched. The focus, sign...</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=362784</comments>
            <pubDate>Fri, 10 Nov 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">362784</guid>        </item>
        <item>
            <title>Differential partitioning of Gαi1 with the cellular microtubules: a possible mechanism of development of Taxol resistance in human ovarian carcinoma cells</title>
            <link>http://www.medworm.com/index.php?rid=362783&amp;cid=s_34078_67_f&amp;fid=34078&amp;url=http%3A%2F%2Fwww.jmolecularsignaling.com%2Fcontent%2F1%2F1%2F3</link>
            <description>Conclusion:
Based on the opposing effects of taxol and the Gαi1 protein on the microtubule dynamic instability (taxol suppresses microtubule dynamic instability whilst the Gαi1 protein inhibits the suppression) our results indicate the operation of a novel pathway that would enable the cells to escape the cytotoxic effects of taxol. (Source: Journal of Molecular Signaling)</description>
            <author>Journal of Molecular Signaling</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=362783</comments>
            <pubDate>Fri, 10 Nov 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">362783</guid>        </item>
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