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10.18632/oncotarget.19111 http://scihub22266oqcxt.onion/10.18632/oncotarget.19111 C5687603!5687603!29179433     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2017 ; 8 (51): 88259-75 Nephropedia Template TP {{tp|p=29179433|t=2017. Regulation of S-formylglutathione hydrolase by the anti-aging gene klotho |pdf=|usr=}}{{29179433}} gab.com Text Regulation of S-formylglutathione hydrolase by the anti-aging gene klotho JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=29179433 #FOAvip Klotho is an aging-suppressor gene. The purpose of this study is to investigate the binding sites (receptors) and function of short-form Klotho (Skl). We showed that Skl physically bound to multiple proteins. We found physical and functional interactions between Skl and S-formylglutathione hydrolase (FGH), a key enzyme in the generation of the major cellular anti-oxidant GSH, using co-immunoprecipitation-coupled mass spectrometry. We further confirmed the colocalization of Skl and FGH around the nucleus in kidney cells using immunofluorescent staining. Skl positively regulated FGH gene expression via Kid3 transcription factor. Overexpression of Skl increased FGH mRNA and protein expression while silencing of Skl attenuated FGH mRNA and protein expression. Klotho gene mutation suppressed FGH expression in red blood cells and kidneys resulting in anemia and kidney damage in mice. Overexpression of Skl increased total GSH production and the GSH/GSSG ratio, an index of anti-oxidant capacity, leading to a decrease in intracellular H2O2 and superoxide levels. The antioxidant activity of Skl was eliminated by silencing of FGH, indicating that Skl increased GSH via FGH. Interestingly, Skl directly interacted with FGH and regulated its function. Site-directed mutagenesis of the N-glycan-modified residues in Skl abolished its antioxidant activity, suggesting that these N-glycan moieties are important features that interact with FGH. Specific mutation of Asp to Ala at site 285 resulted in a loss of anti-oxidant activity of Skl, suggesting that N-glycosylation at site 285 is the key mechanism that determines Skl activity. Therefore, this study demonstrates, for the first time, that Skl regulates anti-oxidant GSH generation via interaction with FGH through N-glycosylation. Twit Text FOAVip Regulation of S-formylglutathione hydrolase by the anti-aging gene klotho ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=29179433 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29179433 #FOAvip English Wikipedia <ref>{{Cite pmid|29179433}}</ref> Regulation of S-formylglutathione hydrolase by the anti-aging gene klotho #MMPMID29179433 Xu Y; Sun Z Oncotarget 2017[Oct]; 8 (51): 88259-75 PMID29179433show ga Klotho is an aging-suppressor gene. The purpose of this study is to investigate the binding sites (receptors) and function of short-form Klotho (Skl). We showed that Skl physically bound to multiple proteins. We found physical and functional interactions between Skl and S-formylglutathione hydrolase (FGH), a key enzyme in the generation of the major cellular anti-oxidant GSH, using co-immunoprecipitation-coupled mass spectrometry. We further confirmed the colocalization of Skl and FGH around the nucleus in kidney cells using immunofluorescent staining. Skl positively regulated FGH gene expression via Kid3 transcription factor. Overexpression of Skl increased FGH mRNA and protein expression while silencing of Skl attenuated FGH mRNA and protein expression. Klotho gene mutation suppressed FGH expression in red blood cells and kidneys resulting in anemia and kidney damage in mice. Overexpression of Skl increased total GSH production and the GSH/GSSG ratio, an index of anti-oxidant capacity, leading to a decrease in intracellular H2O2 and superoxide levels. The antioxidant activity of Skl was eliminated by silencing of FGH, indicating that Skl increased GSH via FGH. Interestingly, Skl directly interacted with FGH and regulated its function. Site-directed mutagenesis of the N-glycan-modified residues in Skl abolished its antioxidant activity, suggesting that these N-glycan moieties are important features that interact with FGH. Specific mutation of Asp to Ala at site 285 resulted in a loss of anti-oxidant activity of Skl, suggesting that N-glycosylation at site 285 is the key mechanism that determines Skl activity. Therefore, this study demonstrates, for the first time, that Skl regulates anti-oxidant GSH generation via interaction with FGH through N-glycosylation. äRegulation of S-formylglutathione hydrolase by the anti-aging gene klo(epmc).pdf DeepDyve Pubget Overpricing