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10.1038/s41598-018-23278-6 http://scihub22266oqcxt.onion/10.1038/s41598-018-23278-6 C5864960!5864960!29567961     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2018 ; 8 (ä): ä Nephropedia Template TP {{tp|p=29567961|t=2018. Rac1 in podocytes promotes glomerular repair and limits the formation of sclerosis |pdf=|usr=}}{{29567961}} gab.com Text Rac1 in podocytes promotes glomerular repair and limits the formation of sclerosis JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=29567961 #FOAvip Rac1, a Rho family member, is ubiquitously expressed and participates in various biological processes. Rac1 expression is induced early in podocyte injury, but its role in repair is unclear. To investigate the role of Rac1 expression in podocytes under pathological conditions, we used podocyte-specific Rac1 conditional knock-out (cKO) mice administered adriamycin (ADR), which causes nephrosis and glomerulosclerosis. Larger areas of detached podocytes, more adhesion of the GBM to Bowman?s capsule, and a higher ratio of sclerotic glomeruli were observed in Rac1 cKO mice than in control mice, whereas no differences were observed in glomerular podocyte numbers in both groups after ADR treatment. The mammalian target of rapamycin (mTOR) pathway, which regulates the cell size, was more strongly suppressed in the podocytes of Rac1 cKO mice than in those of control mice under pathological conditions. In accordance with this result, the volumes of podocytes in Rac1 cKO mice were significantly reduced compared with those of control mice. Experiments using in vitro ADR-administered Rac1 knockdown podocytes also supported that a reduction in Rac1 suppressed mTOR activity in injured podocytes. Taken together, these data indicate that Rac1-associated mTOR activation in podocytes plays an important role in preventing the kidneys from developing glomerulosclerosis. Twit Text FOAVip Rac1 in podocytes promotes glomerular repair and limits the formation of sclerosis ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=29567961 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29567961 #FOAvip English Wikipedia <ref>{{Cite pmid|29567961}}</ref> Rac1 in podocytes promotes glomerular repair and limits the formation of sclerosis #MMPMID29567961 Asao R; Seki T; Takagi M; Yamada H; Kodama F; Hosoe-Nagai Y; Tanaka E; Trejo JAO; Yamamoto-Nonaka K; Sasaki Y; Hidaka T; Ueno T; Yanagita M; Suzuki Y; Tomino Y; Asanuma K Sci Rep 2018[]; 8 (ä): ä PMID29567961show ga Rac1, a Rho family member, is ubiquitously expressed and participates in various biological processes. Rac1 expression is induced early in podocyte injury, but its role in repair is unclear. To investigate the role of Rac1 expression in podocytes under pathological conditions, we used podocyte-specific Rac1 conditional knock-out (cKO) mice administered adriamycin (ADR), which causes nephrosis and glomerulosclerosis. Larger areas of detached podocytes, more adhesion of the GBM to Bowman?s capsule, and a higher ratio of sclerotic glomeruli were observed in Rac1 cKO mice than in control mice, whereas no differences were observed in glomerular podocyte numbers in both groups after ADR treatment. The mammalian target of rapamycin (mTOR) pathway, which regulates the cell size, was more strongly suppressed in the podocytes of Rac1 cKO mice than in those of control mice under pathological conditions. In accordance with this result, the volumes of podocytes in Rac1 cKO mice were significantly reduced compared with those of control mice. Experiments using in vitro ADR-administered Rac1 knockdown podocytes also supported that a reduction in Rac1 suppressed mTOR activity in injured podocytes. Taken together, these data indicate that Rac1-associated mTOR activation in podocytes plays an important role in preventing the kidneys from developing glomerulosclerosis. äRac1 in podocytes promotes glomerular repair and limits the formation (epmc).pdf DeepDyve Pubget Overpricing