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10.4049/jimmunol.1400653 http://scihub22266oqcxt.onion/10.4049/jimmunol.1400653 C4047670!4047670!24778451     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24778451&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 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 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2014 ; 192 (11): 5296-304 Nephropedia Template TP {{tp|p=24778451|t=2014. Endothelial PINK1 mediates the protective effects of NLRP3 deficiency during lethal oxidant injury |pdf=|usr=}}{{24778451}} gab.com Text Endothelial PINK1 mediates the protective effects of NLRP3 deficiency during lethal oxidant injury JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24778451 #FOAvip High levels of inspired oxygen, hyperoxia, are frequently used in patients with acute respiratory failure. Hyperoxia can exacerbate acute respiratory failure, which has high mortality and no specific therapies. We identified a novel roles for PINK1 (PTEN-induced putative kinase 1), a mitochondrial protein, and the cytosolic innate immune protein, NLRP3, in the lung and endothelium. We generated double knockouts (PINK1?/?/NLRP3?/?) as well as cell-targeted PINK1 silencing and lung-targeted overexpression constructs to specifically show that PINK1 mediates cytoprotection in wild type (WT) and NLRP3?/? mice. The ability to resist hyperoxia is proportional to PINK1 expression ? PINK1?/? mice were the most susceptible, WT mice, which induced PINK1 after hyperoxia, had intermediate susceptibility and NLRP3?/? mice, which had high basal and hyperoxia-induced PINK1, were the least susceptible. Genetic deletion of PINK1 or PINK1 silencing in the lung endothelium increased susceptibility to hyperoxia via alterations in autophagy/mitophagy, proteasome activation, apoptosis and oxidant generation. Twit Text FOAVip Endothelial PINK1 mediates the protective effects of NLRP3 deficiency during lethal oxidant injury ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24778451 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24778451 #FOAvip English Wikipedia <ref>{{Cite pmid|24778451}}</ref> Endothelial PINK1 mediates the protective effects of NLRP3 deficiency during lethal oxidant injury #MMPMID24778451 Zhang Y; Sauler M; Shinn AS; Gong H; Haslip M; Shan P; Mannam P; Lee PJ J Immunol 2014[Jun]; 192 (11): 5296-304 PMID24778451show ga High levels of inspired oxygen, hyperoxia, are frequently used in patients with acute respiratory failure. Hyperoxia can exacerbate acute respiratory failure, which has high mortality and no specific therapies. We identified a novel roles for PINK1 (PTEN-induced putative kinase 1), a mitochondrial protein, and the cytosolic innate immune protein, NLRP3, in the lung and endothelium. We generated double knockouts (PINK1?/?/NLRP3?/?) as well as cell-targeted PINK1 silencing and lung-targeted overexpression constructs to specifically show that PINK1 mediates cytoprotection in wild type (WT) and NLRP3?/? mice. The ability to resist hyperoxia is proportional to PINK1 expression ? PINK1?/? mice were the most susceptible, WT mice, which induced PINK1 after hyperoxia, had intermediate susceptibility and NLRP3?/? mice, which had high basal and hyperoxia-induced PINK1, were the least susceptible. Genetic deletion of PINK1 or PINK1 silencing in the lung endothelium increased susceptibility to hyperoxia via alterations in autophagy/mitophagy, proteasome activation, apoptosis and oxidant generation. äEndothelial PINK1 mediates the protective effects of NLRP3 deficiency (epmc).pdf DeepDyve Pubget Overpricing