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10.1038/s41419-017-0002-y http://scihub22266oqcxt.onion/10.1038/s41419-017-0002-y C5870601!5870601!29233968     free     free     free 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 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Dis 2017 ; 8 (12): ä Nephropedia Template TP {{tp|p=29233968|t=2017. HRD1 prevents apoptosis in renal tubular epithelial cells by mediating eIF2? ubiquitylation and degradation |pdf=|usr=}}{{29233968}} gab.com Text HRD1 prevents apoptosis in renal tubular epithelial cells by mediating eIF2 ubiquitylation and degradation JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29233968 #FOAvip Apoptosis of renal tubular epithelial cells is a key feature of the pathogenicity associated with tubulointerstitial fibrosis and other kidney diseases. One factor that regulates important cellular processes like apoptosis and cell proliferation is HRD1, an E3 ubiquitin ligase that acts by promoting ubiquitylation and degradation of its target protein. However, the detailed mechanisms by which HRD1 acts as a regulator of apoptosis in renal tubular epithelial cells have not been established. In our previous liquid chromatography-tandem mass spectrometry (LC-MS/MS) study (Mol Endocrinol. 2016;30:600?613), we demonstrated that one substrate of HRD1 was eIF2?, a critical protein in the PERK-eIF2?-ATF4-CHOP signaling pathway of endoplasmic reticulum (ER) stress. Here, we show that eIF2? expression was increased and HRD1 expression decreased when apoptosis was induced in HKC-8 cells by palmitic acid (PA) or high glucose (HG). HRD1 expression was also lower in kidney tissues from mice with diabetic nephropathy (DN) than in control mice. Forced expression of HRD1 also inhibited apoptosis in HKC-8 cells, while HRD1 overexpression decreased the expression of phosphorylated eIF2? and eIF2?. Further analysis indicated that HRD1 interacted with eIF2? and promoted its ubiquitylation and degradation by the proteasome. Moreover, the HRD1 protection of PA-treated HKC-8 cells was blunted by transfection with Myc-eIF2?. Thus, eIF2? ubiquitylation by HRD1 protects tubular epithelial cells from apoptosis caused by HG and PA, indicating a novel upstream target for therapeutic prevention of renal tubulointerstitial injury. Twit Text FOAVip HRD1 prevents apoptosis in renal tubular epithelial cells by mediating eIF2 ubiquitylation and degradation ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29233968 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29233968 #FOAvip English Wikipedia <ref>{{Cite pmid|29233968}}</ref> HRD1 prevents apoptosis in renal tubular epithelial cells by mediating eIF2? ubiquitylation and degradation #MMPMID29233968 Huang Y; Sun Y; Cao Y; Sun H; Li M; You H; Su D; Li Y; Liang X Cell Death Dis 2017[Dec]; 8 (12): ä PMID29233968show ga Apoptosis of renal tubular epithelial cells is a key feature of the pathogenicity associated with tubulointerstitial fibrosis and other kidney diseases. One factor that regulates important cellular processes like apoptosis and cell proliferation is HRD1, an E3 ubiquitin ligase that acts by promoting ubiquitylation and degradation of its target protein. However, the detailed mechanisms by which HRD1 acts as a regulator of apoptosis in renal tubular epithelial cells have not been established. In our previous liquid chromatography-tandem mass spectrometry (LC-MS/MS) study (Mol Endocrinol. 2016;30:600?613), we demonstrated that one substrate of HRD1 was eIF2?, a critical protein in the PERK-eIF2?-ATF4-CHOP signaling pathway of endoplasmic reticulum (ER) stress. Here, we show that eIF2? expression was increased and HRD1 expression decreased when apoptosis was induced in HKC-8 cells by palmitic acid (PA) or high glucose (HG). HRD1 expression was also lower in kidney tissues from mice with diabetic nephropathy (DN) than in control mice. Forced expression of HRD1 also inhibited apoptosis in HKC-8 cells, while HRD1 overexpression decreased the expression of phosphorylated eIF2? and eIF2?. Further analysis indicated that HRD1 interacted with eIF2? and promoted its ubiquitylation and degradation by the proteasome. Moreover, the HRD1 protection of PA-treated HKC-8 cells was blunted by transfection with Myc-eIF2?. Thus, eIF2? ubiquitylation by HRD1 protects tubular epithelial cells from apoptosis caused by HG and PA, indicating a novel upstream target for therapeutic prevention of renal tubulointerstitial injury. äHRD1 prevents apoptosis in renal tubular epithelial cells by mediating(epmc).pdf DeepDyve Pubget Overpricing