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10.1016/j.ajpath.2015.02.003 http://scihub22266oqcxt.onion/10.1016/j.ajpath.2015.02.003 C4419204!4419204!25759266     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 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 261.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 261.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Pathol 2015 ; 185 (5): 1207-15 Nephropedia Template TP {{tp|p=25759266|t=2015. Kidney Injury Molecule-1 Protects against G?12 Activation and Tissue Damage in Renal Ischemia-Reperfusion Injury |pdf=|usr=}}{{25759266}} gab.com Text Kidney Injury Molecule-1 Protects against G 12 Activation and Tissue Damage in Renal Ischemia-Reperfusion Injury JO: Am J Pathol http://www.kidney.de/pget.php?&tw=1&pmid=25759266 #FOAvip Ischemic acute kidney injury is a serious untreatable condition. Activation of the G protein ?12 (G?12) subunit by reactive oxygen species is a major cause of tissue damage during renal ischemia-reperfusion injury. Kidney injury molecule-1 (KIM-1) is a transmembrane glycoprotein that is highly up-regulated during acute kidney injury, but the physiologic significance of this up-regulation is unclear. Here, we report for the first time that Kim-1 inhibits G?12 activation and protects mice against renal ischemia-reperfusion injury. We reveal that Kim-1 physically interacts with and inhibits cellular G?12 activation after inflammatory stimuli, including reactive oxygen species, by blocking GTP binding to G?12. Compared with Kim-1+/+ mice, Kim-1?/? mice exhibited greater G?12 and downstream Src activation both in primary tubular epithelial cells after in vitro stimulation with H2O2 and in whole kidneys after unilateral renal artery clamping. Finally, we show that Kim-1?deficient mice had more severe kidney dysfunction and tissue damage after bilateral renal artery clamping, compared with wild-type mice. Our results suggest that KIM-1 is an endogenous protective mechanism against renal ischemia-reperfusion injury through inhibition of G?12. Twit Text FOAVip Kidney Injury Molecule-1 Protects against G 12 Activation and Tissue Damage in Renal Ischemia-Reperfusion Injury ????Am J Pathol http://www.kidney.de/pget.php?&tw=1&pmid=25759266 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25759266 #FOAvip English Wikipedia <ref>{{Cite pmid|25759266}}</ref> Kidney Injury Molecule-1 Protects against G?12 Activation and Tissue Damage in Renal Ischemia-Reperfusion Injury #MMPMID25759266 Ismail OZ; Zhang X; Wei J; Haig A; Denker BM; Suri RS; Sener A; Gunaratnam L Am J Pathol 2015[May]; 185 (5): 1207-15 PMID25759266show ga Ischemic acute kidney injury is a serious untreatable condition. Activation of the G protein ?12 (G?12) subunit by reactive oxygen species is a major cause of tissue damage during renal ischemia-reperfusion injury. Kidney injury molecule-1 (KIM-1) is a transmembrane glycoprotein that is highly up-regulated during acute kidney injury, but the physiologic significance of this up-regulation is unclear. Here, we report for the first time that Kim-1 inhibits G?12 activation and protects mice against renal ischemia-reperfusion injury. We reveal that Kim-1 physically interacts with and inhibits cellular G?12 activation after inflammatory stimuli, including reactive oxygen species, by blocking GTP binding to G?12. Compared with Kim-1+/+ mice, Kim-1?/? mice exhibited greater G?12 and downstream Src activation both in primary tubular epithelial cells after in vitro stimulation with H2O2 and in whole kidneys after unilateral renal artery clamping. Finally, we show that Kim-1?deficient mice had more severe kidney dysfunction and tissue damage after bilateral renal artery clamping, compared with wild-type mice. Our results suggest that KIM-1 is an endogenous protective mechanism against renal ischemia-reperfusion injury through inhibition of G?12. äKidney Injury Molecule-1 Protects against G?12 Activation and Tissue D(epmc).pdf DeepDyve Pubget Overpricing