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10.1091/mbc.e10-01-0055 http://scihub22266oqcxt.onion/10.1091/mbc.e10-01-0055 20357001!2869375!20357001     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=20357001&cmd=llinks): Failed to open stream: HTTP request failed! 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Regulation of lens gap junctions by Transforming Growth Factor beta |pdf=|usr=}}{{20357001}} gab.com Text Regulation of lens gap junctions by Transforming Growth Factor beta JO: Mol Biol Cell http://www.kidney.de/pget.php?&tw=1&pmid=20357001 #FOAvip Gap junction-mediated intercellular communication (GJIC) is essential for the proper function of many organs, including the lens. GJIC in lens epithelial cells is increased by FGF in a concentration-dependent process that has been linked to the intralenticular gradient of GJIC required for lens transparency. Unlike FGF, elevated levels of TGF-beta are associated with lens dysfunction. We show that TGF-beta1 or -2 up-regulates dye coupling in serum-free primary cultures of chick lens epithelial cells (dissociated cell-derived monolayer cultures [DCDMLs]) via a mechanism distinct from that utilized by other growth factors. Remarkably, the ability of TGF-beta and of FGF to up-regulate GJIC is abolished if DCDMLs are simultaneously exposed to both factors despite undiminished cell-cell contact. This reduction in dye coupling is attributable to an inhibition of gap junction assembly. Connexin 45.6, 43, and 56-containing gap junctions are restored, and intercellular dye coupling is increased, if the activity of p38 kinase is blocked. Our data reveal a new type of cross-talk between the FGF and TGF-beta pathways, as well as a novel role for TGF-beta and p38 kinase in the regulation of GJIC. They also provide an explanation for how pathologically increased TGF-beta signaling could contribute to cataract formation. Twit Text FOAVip Regulation of lens gap junctions by Transforming Growth Factor beta ????Mol Biol Cell http://www.kidney.de/pget.php?&tw=1&pmid=20357001 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=20357001 #FOAvip English Wikipedia <ref>{{Cite pmid|20357001}}</ref> Regulation of lens gap junctions by Transforming Growth Factor beta #MMPMID20357001 Boswell BA; VanSlyke JK; Musil LS Mol Biol Cell 2010[May]; 21 (10): 1686-97 PMID20357001show ga Gap junction-mediated intercellular communication (GJIC) is essential for the proper function of many organs, including the lens. GJIC in lens epithelial cells is increased by FGF in a concentration-dependent process that has been linked to the intralenticular gradient of GJIC required for lens transparency. Unlike FGF, elevated levels of TGF-beta are associated with lens dysfunction. We show that TGF-beta1 or -2 up-regulates dye coupling in serum-free primary cultures of chick lens epithelial cells (dissociated cell-derived monolayer cultures [DCDMLs]) via a mechanism distinct from that utilized by other growth factors. Remarkably, the ability of TGF-beta and of FGF to up-regulate GJIC is abolished if DCDMLs are simultaneously exposed to both factors despite undiminished cell-cell contact. This reduction in dye coupling is attributable to an inhibition of gap junction assembly. Connexin 45.6, 43, and 56-containing gap junctions are restored, and intercellular dye coupling is increased, if the activity of p38 kinase is blocked. Our data reveal a new type of cross-talk between the FGF and TGF-beta pathways, as well as a novel role for TGF-beta and p38 kinase in the regulation of GJIC. They also provide an explanation for how pathologically increased TGF-beta signaling could contribute to cataract formation. |Animals[MESH] |Cell Communication/drug effects/physiology[MESH] |Chick Embryo[MESH] |Connexins[MESH] |Embryo, Nonmammalian/cytology/metabolism[MESH] |Epithelial Cells/metabolism[MESH] |Fibroblast Growth Factors/metabolism/physiology[MESH] |Gap Junctions/*metabolism/physiology[MESH] |Lens, Crystalline/*cytology/metabolism[MESH] |Signal Transduction/drug effects[MESH] |Transforming Growth Factor beta/metabolism/*pharmacology[MESH] |Transforming Growth Factor beta1/metabolism[MESH]Regulation of lens gap junctions by Transforming Growth Factor beta (epmc).pdf DeepDyve Pubget Overpricing