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10.1074/jbc.M115.713123 http://scihub22266oqcxt.onion/10.1074/jbc.M115.713123 C4777869!4777869!26763233     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       J+Biol+Chem 2016 ; 291 (10): 5396-405 Nephropedia Template TP {{tp|p=26763233|t=2016. Loss of ?-Tubulin Acetylation Is Associated with TGF-?-induced Epithelial-Mesenchymal Transition* |pdf=|usr=}}{{26763233}} gab.com Text Loss of -Tubulin Acetylation Is Associated with TGF- -induced Epithelial-Mesenchymal Transition* JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=26763233 #FOAvip The epithelial-to-mesenchymal transition (EMT) is a process by which differentiated epithelial cells reprogram gene expression, lose their junctions and polarity, reorganize their cytoskeleton, increase cell motility and assume a mesenchymal morphology. Despite the critical functions of the microtubule (MT) in cytoskeletal organization, how it participates in EMT induction and maintenance remains poorly understood. Here we report that acetylated ?-tubulin, which plays an important role in microtubule (MT) stabilization and cell morphology, can serve as a novel regulator and marker of EMT. A high level of acetylated ?-tubulin was correlated with epithelial morphology and it profoundly decreased during TGF-?-induced EMT. We found that TGF-? increased the activity of HDAC6, a major deacetylase of ?-tubulin, without affecting its expression levels. Treatment with HDAC6 inhibitor tubacin or TGF-? type I receptor inhibitor SB431542 restored the level of acetylated ?-tubulin and consequently blocked EMT. Our results demonstrate that acetylated ?-tubulin can serve as a marker of EMT and that HDAC6 represents an important regulator during EMT process. Twit Text FOAVip Loss of -Tubulin Acetylation Is Associated with TGF- -induced Epithelial-Mesenchymal Transition* ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=26763233 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26763233 #FOAvip English Wikipedia <ref>{{Cite pmid|26763233}}</ref> Loss of ?-Tubulin Acetylation Is Associated with TGF-?-induced Epithelial-Mesenchymal Transition* #MMPMID26763233 Gu S; Liu Y; Zhu B; Ding K; Yao TP; Chen F; Zhan L; Xu P; Ehrlich M; Liang T; Lin X; Feng XH J Biol Chem 2016[Mar]; 291 (10): 5396-405 PMID26763233show ga The epithelial-to-mesenchymal transition (EMT) is a process by which differentiated epithelial cells reprogram gene expression, lose their junctions and polarity, reorganize their cytoskeleton, increase cell motility and assume a mesenchymal morphology. Despite the critical functions of the microtubule (MT) in cytoskeletal organization, how it participates in EMT induction and maintenance remains poorly understood. Here we report that acetylated ?-tubulin, which plays an important role in microtubule (MT) stabilization and cell morphology, can serve as a novel regulator and marker of EMT. A high level of acetylated ?-tubulin was correlated with epithelial morphology and it profoundly decreased during TGF-?-induced EMT. We found that TGF-? increased the activity of HDAC6, a major deacetylase of ?-tubulin, without affecting its expression levels. Treatment with HDAC6 inhibitor tubacin or TGF-? type I receptor inhibitor SB431542 restored the level of acetylated ?-tubulin and consequently blocked EMT. Our results demonstrate that acetylated ?-tubulin can serve as a marker of EMT and that HDAC6 represents an important regulator during EMT process. äLoss of ?-Tubulin Acetylation Is Associated with TGF-?-induced Epithel(epmc).pdf DeepDyve Pubget Overpricing