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10.1096/fj.14-262527 http://scihub22266oqcxt.onion/10.1096/fj.14-262527 C4396616!4396616!25480384     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25480384.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       FASEB+J 2015 ; 29 (4): 1258-68 Nephropedia Template TP {{tp|p=25480384|t=2015. Tumor suppressor ataxia telangiectasia mutated functions downstream of TGF-?1 in orchestrating profibrotic responses |pdf=|usr=}}{{25480384}} gab.com Text Tumor suppressor ataxia telangiectasia mutated functions downstream of TGF- 1 in orchestrating profibrotic responses JO: FASEB J http://www.kidney.de/pget.php?&tw=1&pmid=25480384 #FOAvip Effective therapy to prevent organ fibrosis, which is associated with more than half of all mortalities, remains elusive. Involvement of tumor suppressor ataxia telangiectasia mutated (ATM) in the TGF-?1 pathway related to renal fibrosis is largely unknown. ATM activation (pATMSer1981) increased 4-fold in the tubulointerstitial region of the unilateral ureteral obstruction-injured kidney in mice correlating with SMAD3 and p53Ser15 phosphorylation and elevated levels of p22phox subunit of the NADPH oxidases (NOXs), and fibrotic markers, plasminogen activator inhibitor-1 (PAI-1), and fibronectin, when compared to contralateral (contra) or sham controls. In fact, ATM is rapidly phosphorylated at Ser1981 by TGF-?1 stimulation. Stable silencing and pharmacologic inhibition of ATM ablated TGF-?1?induced p53 activation (>95%) and subsequent PAI-1, fibronectin, connective tissue growth factor, and p21 expression in human kidney 2 (HK-2) tubular epithelial cells and normal rat kidney-49 fibroblasts (NRK-49F). ATM or p53 depletion in HK-2 cells, moreover, bypassed TGF-?1?mediated cytostasis evident in control short hairpin RNA-expressing HK-2 cells. Interestingly, stable silencing of NOX subunits, p22phox and p47phox, in HK-2 cells blocked TGF-?1-induced pATMSer1981 (>90%) and target gene induction via p53-dependent mechanisms. Furthermore, NRK-49F fibroblast proliferation triggered by conditioned media from TGF-?1?stimulated, control vector-transfected HK-2 cells decreased (?50%) when exposed to conditioned media from ATM-deficient, TGF-?1?treated HK-2 cells. Thus, TGF-?1 promotes NOX-dependent ATM activation leading to p53-mediated fibrotic gene reprogramming and growth arrest in HK-2 cells. Furthermore, TGF-?1/ATM-initiated paracrine factor secretion by dysfunctional renal epithelium promotes interstitial fibroblast growth, suggesting a role of tubular ATM in mediating epithelial-mesenchymal cross-talk highlighting the translational benefit of targeting the NOX/ATM/p53 axis in renal fibrosis.?Overstreet, J. M., Samarakoon, R., Cardona-Grau, D., Goldschmeding, R., Higgins, P. J. Tumor suppressor ataxia telangiectasia mutated functions downstream of TGF-?1 in orchestrating profibrotic responses. Twit Text FOAVip Tumor suppressor ataxia telangiectasia mutated functions downstream of TGF- 1 in orchestrating profibrotic responses ????FASEB J http://www.kidney.de/pget.php?&tw=1&pmid=25480384 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25480384 #FOAvip English Wikipedia <ref>{{Cite pmid|25480384}}</ref> Tumor suppressor ataxia telangiectasia mutated functions downstream of TGF-?1 in orchestrating profibrotic responses #MMPMID25480384 Overstreet JM; Samarakoon R; Cardona-Grau D; Goldschmeding R; Higgins PJ FASEB J 2015[Apr]; 29 (4): 1258-68 PMID25480384show ga Effective therapy to prevent organ fibrosis, which is associated with more than half of all mortalities, remains elusive. Involvement of tumor suppressor ataxia telangiectasia mutated (ATM) in the TGF-?1 pathway related to renal fibrosis is largely unknown. ATM activation (pATMSer1981) increased 4-fold in the tubulointerstitial region of the unilateral ureteral obstruction-injured kidney in mice correlating with SMAD3 and p53Ser15 phosphorylation and elevated levels of p22phox subunit of the NADPH oxidases (NOXs), and fibrotic markers, plasminogen activator inhibitor-1 (PAI-1), and fibronectin, when compared to contralateral (contra) or sham controls. In fact, ATM is rapidly phosphorylated at Ser1981 by TGF-?1 stimulation. Stable silencing and pharmacologic inhibition of ATM ablated TGF-?1?induced p53 activation (>95%) and subsequent PAI-1, fibronectin, connective tissue growth factor, and p21 expression in human kidney 2 (HK-2) tubular epithelial cells and normal rat kidney-49 fibroblasts (NRK-49F). ATM or p53 depletion in HK-2 cells, moreover, bypassed TGF-?1?mediated cytostasis evident in control short hairpin RNA-expressing HK-2 cells. Interestingly, stable silencing of NOX subunits, p22phox and p47phox, in HK-2 cells blocked TGF-?1-induced pATMSer1981 (>90%) and target gene induction via p53-dependent mechanisms. Furthermore, NRK-49F fibroblast proliferation triggered by conditioned media from TGF-?1?stimulated, control vector-transfected HK-2 cells decreased (?50%) when exposed to conditioned media from ATM-deficient, TGF-?1?treated HK-2 cells. Thus, TGF-?1 promotes NOX-dependent ATM activation leading to p53-mediated fibrotic gene reprogramming and growth arrest in HK-2 cells. Furthermore, TGF-?1/ATM-initiated paracrine factor secretion by dysfunctional renal epithelium promotes interstitial fibroblast growth, suggesting a role of tubular ATM in mediating epithelial-mesenchymal cross-talk highlighting the translational benefit of targeting the NOX/ATM/p53 axis in renal fibrosis.?Overstreet, J. M., Samarakoon, R., Cardona-Grau, D., Goldschmeding, R., Higgins, P. J. Tumor suppressor ataxia telangiectasia mutated functions downstream of TGF-?1 in orchestrating profibrotic responses. äTumor suppressor ataxia telangiectasia mutated functions downstream of(epmc).pdf DeepDyve Pubget Overpricing