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10.1038/srep25785 http://scihub22266oqcxt.onion/10.1038/srep25785 C4865757!4865757!27173636     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 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=27173636|t=2016. Identification of P-Rex1 as an anti-inflammatory and anti-fibrogenic target for pulmonary fibrosis |pdf=|usr=}}{{27173636}} gab.com Text Identification of P-Rex1 as an anti-inflammatory and anti-fibrogenic target for pulmonary fibrosis JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27173636 #FOAvip Pulmonary fibrosis (PF) leads to progressive and often irreversible loss of lung functions, posing a health threat with no effective cure. We examined P-Rex1, a PI3K- and G protein ??-regulated guanine nucleotide exchange factor (GEF) of the Rac small GTPase, for its potential involvement in PF. In a bleomycin-induced PF model, mice deficient in p-rex1 had well-preserved alveolar structure and survived significantly better than their wild type (WT) littermates. The p-rex1?/? mice expressed significantly less proinflammatory cytokines and chemokines and had reduced leukocyte infiltration in the lung tissue than their WT littermates. P-Rex1 was detected in lung fibroblasts of WT mice, and its genetic deletion attenuated TGF?-1-stimulated lung fibroblast migration, Rac1 activation and p38 MAPK phosphorylation. The p-rex1?/? mice showed significantly reduced pathological changes including the expression of ?-smooth muscle actin, fibronectin and TGF?-1 compared with their WT controls. Expression of a GEF-deficient P-Rex1 mutant effectively blocked Smads-dependent transcriptional activation, suggesting that P-Rex1 is a downstream mediator of TGF?-1 signaling. These findings identify P-Rex1 as a novel player of PF, suggesting that targeting P-Rex1 may simultaneously block the inflammatory and fibrogenic processes of PF. Twit Text FOAVip Identification of P-Rex1 as an anti-inflammatory and anti-fibrogenic target for pulmonary fibrosis ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27173636 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27173636 #FOAvip English Wikipedia <ref>{{Cite pmid|27173636}}</ref> Identification of P-Rex1 as an anti-inflammatory and anti-fibrogenic target for pulmonary fibrosis #MMPMID27173636 Liang Q; Cheng N; Zhang G; Liang Y; Qian F; Wu D; Ye RD Sci Rep 2016[]; 6 (ä): ä PMID27173636show ga Pulmonary fibrosis (PF) leads to progressive and often irreversible loss of lung functions, posing a health threat with no effective cure. We examined P-Rex1, a PI3K- and G protein ??-regulated guanine nucleotide exchange factor (GEF) of the Rac small GTPase, for its potential involvement in PF. In a bleomycin-induced PF model, mice deficient in p-rex1 had well-preserved alveolar structure and survived significantly better than their wild type (WT) littermates. The p-rex1?/? mice expressed significantly less proinflammatory cytokines and chemokines and had reduced leukocyte infiltration in the lung tissue than their WT littermates. P-Rex1 was detected in lung fibroblasts of WT mice, and its genetic deletion attenuated TGF?-1-stimulated lung fibroblast migration, Rac1 activation and p38 MAPK phosphorylation. The p-rex1?/? mice showed significantly reduced pathological changes including the expression of ?-smooth muscle actin, fibronectin and TGF?-1 compared with their WT controls. Expression of a GEF-deficient P-Rex1 mutant effectively blocked Smads-dependent transcriptional activation, suggesting that P-Rex1 is a downstream mediator of TGF?-1 signaling. These findings identify P-Rex1 as a novel player of PF, suggesting that targeting P-Rex1 may simultaneously block the inflammatory and fibrogenic processes of PF. äIdentification of P-Rex1 as an anti-inflammatory and anti-fibrogenic t(epmc).pdf DeepDyve Pubget Overpricing