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10.1371/journal.pbio.1002325 http://scihub22266oqcxt.onion/10.1371/journal.pbio.1002325 C4682977!4682977!26680585     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+Biol 2015 ; 13 (12): ä Nephropedia Template TP {{tp|p=26680585|t=2015. ShcA Protects against Epithelial?Mesenchymal Transition through Compartmentalized Inhibition of TGF-?-Induced Smad Activation |pdf=|usr=}}{{26680585}} gab.com Text ShcA Protects against Epithelial Mesenchymal Transition through Compartmentalized Inhibition of TGF- -Induced Smad Activation JO: PLoS Biol http://www.kidney.de/pget.php?&tw=1&pmid=26680585 #FOAvip Epithelial?mesenchymal transition (EMT) is a normal cell differentiation event during development and contributes pathologically to carcinoma and fibrosis progression. EMT often associates with increased transforming growth factor-? (TGF-?) signaling, and TGF-? drives EMT, in part through Smad-mediated reprogramming of gene expression. TGF-? also activates the Erk MAPK pathway through recruitment and Tyr phosphorylation of the adaptor protein ShcA by the activated TGF-? type I receptor. We found that ShcA protects the epithelial integrity of nontransformed cells against EMT by repressing TGF-?-induced, Smad-mediated gene expression. p52ShcA competed with Smad3 for TGF-? receptor binding, and down-regulation of ShcA expression enhanced autocrine TGF-?/Smad signaling and target gene expression, whereas increased p52ShcA expression resulted in decreased Smad3 binding to the TGF-? receptor, decreased Smad3 activation, and increased Erk MAPK and Akt signaling. Furthermore, p52ShcA sequestered TGF-? receptor complexes to caveolin-associated membrane compartments, and reducing ShcA expression enhanced the receptor localization in clathrin-associated membrane compartments that enable Smad activation. Consequently, silencing ShcA expression induced EMT, with increased cell migration, invasion, and dissemination, and increased stem cell generation and mammosphere formation, dependent upon autocrine TGF-? signaling. These findings position ShcA as a determinant of the epithelial phenotype by repressing TGF-?-induced Smad activation through differential partitioning of receptor complexes at the cell surface. Twit Text FOAVip ShcA Protects against Epithelial Mesenchymal Transition through Compartmentalized Inhibition of TGF- -Induced Smad Activation ????PLoS Biol http://www.kidney.de/pget.php?&tw=1&pmid=26680585 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26680585 #FOAvip English Wikipedia <ref>{{Cite pmid|26680585}}</ref> ShcA Protects against Epithelial?Mesenchymal Transition through Compartmentalized Inhibition of TGF-?-Induced Smad Activation #MMPMID26680585 Muthusamy BP; Budi EH; Katsuno Y; Lee MK; Smith SM; Mirza AM; Akhurst RJ; Derynck R PLoS Biol 2015[Dec]; 13 (12): ä PMID26680585show ga Epithelial?mesenchymal transition (EMT) is a normal cell differentiation event during development and contributes pathologically to carcinoma and fibrosis progression. EMT often associates with increased transforming growth factor-? (TGF-?) signaling, and TGF-? drives EMT, in part through Smad-mediated reprogramming of gene expression. TGF-? also activates the Erk MAPK pathway through recruitment and Tyr phosphorylation of the adaptor protein ShcA by the activated TGF-? type I receptor. We found that ShcA protects the epithelial integrity of nontransformed cells against EMT by repressing TGF-?-induced, Smad-mediated gene expression. p52ShcA competed with Smad3 for TGF-? receptor binding, and down-regulation of ShcA expression enhanced autocrine TGF-?/Smad signaling and target gene expression, whereas increased p52ShcA expression resulted in decreased Smad3 binding to the TGF-? receptor, decreased Smad3 activation, and increased Erk MAPK and Akt signaling. Furthermore, p52ShcA sequestered TGF-? receptor complexes to caveolin-associated membrane compartments, and reducing ShcA expression enhanced the receptor localization in clathrin-associated membrane compartments that enable Smad activation. Consequently, silencing ShcA expression induced EMT, with increased cell migration, invasion, and dissemination, and increased stem cell generation and mammosphere formation, dependent upon autocrine TGF-? signaling. These findings position ShcA as a determinant of the epithelial phenotype by repressing TGF-?-induced Smad activation through differential partitioning of receptor complexes at the cell surface. äShcA Protects against Epithelial?Mesenchymal Transition through Compar(epmc).pdf DeepDyve Pubget Overpricing