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10.18632/oncotarget.7965 http://scihub22266oqcxt.onion/10.18632/oncotarget.7965 C5008374!5008374!26967557     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2016 ; 7 (16): 22474-85 Nephropedia Template TP {{tp|p=26967557|t=2016. MG53 permeates through blood-brain barrier to protect ischemic brain injury |pdf=|usr=}}{{26967557}} gab.com Text MG53 permeates through blood-brain barrier to protect ischemic brain injury JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26967557 #FOAvip Ischemic injury to neurons represents the underlying cause of stroke to the brain. Our previous studies identified MG53 as an essential component of the cell membrane repair machinery. Here we show that the recombinant human (rh)MG53 protein facilitates repair of ischemia-reperfusion (IR) injury to the brain. MG53 rapidly moves to acute injury sites on neuronal cells to form a membrane repair patch. IR-induced brain injury increases permeability of the blood-brain-barrier, providing access of MG53 from blood circulation to target the injured brain tissues. Exogenous rhMG53 protein can protect cultured neurons against hypoxia/reoxygenation-induced damages. Transgenic mice with increased levels of MG53 in the bloodstream are resistant to IR-induced brain injury. Intravenous administration of rhMG53, either prior to or after ischemia, can effectively alleviate brain injuries in rats. rhMG53-mediated neuroprotection involves suppression of apoptotic neuronal cell death, as well as activation of the pro-survival RISK signaling pathway. Our data indicate a physiological function for MG53 in the brain and suggest that targeting membrane repair or RISK signaling may be an effective means to treat ischemic brain injury. Twit Text FOAVip MG53 permeates through blood-brain barrier to protect ischemic brain injury ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26967557 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26967557 #FOAvip English Wikipedia <ref>{{Cite pmid|26967557}}</ref> MG53 permeates through blood-brain barrier to protect ischemic brain injury #MMPMID26967557 Yao Y; Zhang B; Zhu H; Li H; Han Y; Chen K; Wang Z; Zeng J; Liu Y; Wang X; Li Y; He D; Lin P; Zhou X; Park KH; Bian Z; Chen Z; Gong N; Tan T; Zhou J; Zhang M; Ma J; Zeng C Oncotarget 2016[Apr]; 7 (16): 22474-85 PMID26967557show ga Ischemic injury to neurons represents the underlying cause of stroke to the brain. Our previous studies identified MG53 as an essential component of the cell membrane repair machinery. Here we show that the recombinant human (rh)MG53 protein facilitates repair of ischemia-reperfusion (IR) injury to the brain. MG53 rapidly moves to acute injury sites on neuronal cells to form a membrane repair patch. IR-induced brain injury increases permeability of the blood-brain-barrier, providing access of MG53 from blood circulation to target the injured brain tissues. Exogenous rhMG53 protein can protect cultured neurons against hypoxia/reoxygenation-induced damages. Transgenic mice with increased levels of MG53 in the bloodstream are resistant to IR-induced brain injury. Intravenous administration of rhMG53, either prior to or after ischemia, can effectively alleviate brain injuries in rats. rhMG53-mediated neuroprotection involves suppression of apoptotic neuronal cell death, as well as activation of the pro-survival RISK signaling pathway. Our data indicate a physiological function for MG53 in the brain and suggest that targeting membrane repair or RISK signaling may be an effective means to treat ischemic brain injury. äMG53 permeates through blood-brain barrier to protect ischemic brain i(epmc).pdf DeepDyve Pubget Overpricing