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10.1038/srep33116 http://scihub22266oqcxt.onion/10.1038/srep33116 C5015047!5015047!27604640     free     free     free Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 249.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 249.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 249.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 249.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2016 ; 6 (ä): ä Nephropedia Template TP {{tp|p=27604640|t=2016. Ubiquitin carboxyl-terminal hydrolase-L5 promotes TGF?-1 signaling by de-ubiquitinating and stabilizing Smad2/Smad3 in pulmonary fibrosis |pdf=|usr=}}{{27604640}} gab.com Text Ubiquitin carboxyl-terminal hydrolase-L5 promotes TGF -1 signaling by de-ubiquitinating and stabilizing Smad2/Smad3 in pulmonary fibrosis JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27604640 #FOAvip Transforming growth factor ?-1 (TGF?-1)-induced phosphorylation of transcription factors Smad2 and Smad3 plays a crucial role in the pathogenesis of idiopathic pulmonary fibrosis (IPF). However, the molecular regulation of Smad2/Smad3 proteins stability remains a mystery. Here, we show that ubiquitin carboxyl-terminal hydrolase-L5 (UCHL5 or UCH37) de-ubiquitinates both Smad2 and Smad3, up-regulates their stability, and promotes TGF?-1-induced expression of profibrotic proteins, such as fibronectin (FN) and ?-smooth muscle actin (?-SMA). Inhibition or down-regulation of UCHL5 reduced Smad2/Smad3 levels and TGF?-1-induced the expression of FN and ?-SMA in human lung fibroblast. We demonstrate that Smad2 and Smad3 ubiquitination was diminished by over-expression of UCHL5, while it was enhanced by inhibition or down-regulation of UCHL5. UCHL5 is highly expressed in IPF lungs. UCHL5, Smad2, and Smad3 levels were increased in bleomycin-injured lungs. Administration of UCHL5 inhibitor, b-AP15, reduced the expression of FN, type I collagen, Smad2/Smad3, and the deposition of collagen in lung tissues in a bleomycin-induced model of pulmonary fibrosis. Our studies provide a molecular mechanism by which UCHL5 mitigates TGF?-1 signaling by stabilizing Smad2/Smad3. These data indicate that UCHL5 may contribute to the pathogenesis of IPF and may be a potential therapeutic target. Twit Text FOAVip Ubiquitin carboxyl-terminal hydrolase-L5 promotes TGF -1 signaling by de-ubiquitinating and stabilizing Smad2/Smad3 in pulmonary fibrosis ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27604640 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27604640 #FOAvip English Wikipedia <ref>{{Cite pmid|27604640}}</ref> Ubiquitin carboxyl-terminal hydrolase-L5 promotes TGF?-1 signaling by de-ubiquitinating and stabilizing Smad2/Smad3 in pulmonary fibrosis #MMPMID27604640 Nan L; Jacko AM; Tan J; Wang D; Zhao J; Kass DJ; Ma H; Zhao Y Sci Rep 2016[]; 6 (ä): ä PMID27604640show ga Transforming growth factor ?-1 (TGF?-1)-induced phosphorylation of transcription factors Smad2 and Smad3 plays a crucial role in the pathogenesis of idiopathic pulmonary fibrosis (IPF). However, the molecular regulation of Smad2/Smad3 proteins stability remains a mystery. Here, we show that ubiquitin carboxyl-terminal hydrolase-L5 (UCHL5 or UCH37) de-ubiquitinates both Smad2 and Smad3, up-regulates their stability, and promotes TGF?-1-induced expression of profibrotic proteins, such as fibronectin (FN) and ?-smooth muscle actin (?-SMA). Inhibition or down-regulation of UCHL5 reduced Smad2/Smad3 levels and TGF?-1-induced the expression of FN and ?-SMA in human lung fibroblast. We demonstrate that Smad2 and Smad3 ubiquitination was diminished by over-expression of UCHL5, while it was enhanced by inhibition or down-regulation of UCHL5. UCHL5 is highly expressed in IPF lungs. UCHL5, Smad2, and Smad3 levels were increased in bleomycin-injured lungs. Administration of UCHL5 inhibitor, b-AP15, reduced the expression of FN, type I collagen, Smad2/Smad3, and the deposition of collagen in lung tissues in a bleomycin-induced model of pulmonary fibrosis. Our studies provide a molecular mechanism by which UCHL5 mitigates TGF?-1 signaling by stabilizing Smad2/Smad3. These data indicate that UCHL5 may contribute to the pathogenesis of IPF and may be a potential therapeutic target. äUbiquitin carboxyl-terminal hydrolase-L5 promotes TGF?-1 signaling by (epmc).pdf DeepDyve Pubget Overpricing