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10.1128/MCB.00479-16 http://scihub22266oqcxt.onion/10.1128/MCB.00479-16 C5477549!5477549!28242652     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 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Cell+Biol 2017 ; 37 (10): ä Nephropedia Template TP {{tp|p=28242652|t=2017. Glucose Deprivation Induces ATF4-Mediated Apoptosis through TRAIL Death Receptors |pdf=|usr=}}{{28242652}} gab.com Text Glucose Deprivation Induces ATF4-Mediated Apoptosis through TRAIL Death Receptors JO: Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=28242652 #FOAvip Metabolic stress occurs frequently in tumors and in normal tissues undergoing transient ischemia. Nutrient deprivation triggers, among many potential cell death-inducing pathways, an endoplasmic reticulum (ER) stress response with the induction of the integrated stress response transcription factor ATF4. However, how this results in cell death remains unknown. Here we show that glucose deprivation triggered ER stress and induced the unfolded protein response transcription factors ATF4 and CHOP. This was associated with the nontranscriptional accumulation of TRAIL receptor 1 (TRAIL-R1) (DR4) and with the ATF4-mediated, CHOP-independent induction of TRAIL-R2 (DR5), suggesting that cell death in this context may involve death receptor signaling. Consistent with this, the ablation of TRAIL-R1, TRAIL-R2, FADD, Bid, and caspase-8 attenuated cell death, although the downregulation of TRAIL did not, suggesting ligand-independent activation of TRAIL receptors. These data indicate that stress triggered by glucose deprivation promotes the ATF4-dependent upregulation of TRAIL-R2/DR5 and TRAIL receptor-mediated cell death. Twit Text FOAVip Glucose Deprivation Induces ATF4-Mediated Apoptosis through TRAIL Death Receptors ????Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=28242652 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28242652 #FOAvip English Wikipedia <ref>{{Cite pmid|28242652}}</ref> Glucose Deprivation Induces ATF4-Mediated Apoptosis through TRAIL Death Receptors #MMPMID28242652 Iurlaro R; Püschel F; León-Annicchiarico CL; O'Connor H; Martin SJ; Palou-Gramón D; Lucendo E; Muñoz-Pinedo C Mol Cell Biol 2017[May]; 37 (10): ä PMID28242652show ga Metabolic stress occurs frequently in tumors and in normal tissues undergoing transient ischemia. Nutrient deprivation triggers, among many potential cell death-inducing pathways, an endoplasmic reticulum (ER) stress response with the induction of the integrated stress response transcription factor ATF4. However, how this results in cell death remains unknown. Here we show that glucose deprivation triggered ER stress and induced the unfolded protein response transcription factors ATF4 and CHOP. This was associated with the nontranscriptional accumulation of TRAIL receptor 1 (TRAIL-R1) (DR4) and with the ATF4-mediated, CHOP-independent induction of TRAIL-R2 (DR5), suggesting that cell death in this context may involve death receptor signaling. Consistent with this, the ablation of TRAIL-R1, TRAIL-R2, FADD, Bid, and caspase-8 attenuated cell death, although the downregulation of TRAIL did not, suggesting ligand-independent activation of TRAIL receptors. These data indicate that stress triggered by glucose deprivation promotes the ATF4-dependent upregulation of TRAIL-R2/DR5 and TRAIL receptor-mediated cell death. äGlucose Deprivation Induces ATF4-Mediated Apoptosis through TRAIL Deat(epmc).pdf DeepDyve Pubget Overpricing