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10.1194/jlr.M051094 http://scihub22266oqcxt.onion/10.1194/jlr.M051094 C4617134!4617134!25183803     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 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Lipid+Res 2014 ; 55 (11): 2320-33 Nephropedia Template TP {{tp|p=25183803|t=2014. Protein kinase R-like endoplasmic reticulum kinase and glycogen synthase kinase-3?/? regulate foam cell formation S |pdf=|usr=}}{{25183803}} gab.com Text Protein kinase R-like endoplasmic reticulum kinase and glycogen synthase kinase-3 / regulate foam cell formation S JO: J Lipid Res http://www.kidney.de/pget.php?&tw=1&pmid=25183803 #FOAvip Evidence suggests a causative role for endoplasmic reticulum (ER) stress in the development of atherosclerosis. This study investigated the potential role of glycogen synthase kinase (GSK)-3?/? in proatherogenic ER stress signaling. Thp1-derived macrophages were treated with the ER stress-inducing agents, glucosamine, thapsigargin, or palmitate. Using small-molecule inhibitors of specific unfolded protein response (UPR) signaling pathways, we found that protein kinase R-like ER kinase (PERK), but not inositol requiring enzyme 1 or activating transcription factor 6, is required for the activation of GSK3?/? by ER stress. GSK3?/? inhibition or siRNA-directed knockdown attenuated ER stress-induced expression of distal components of the PERK pathway. Macrophage foam cells within atherosclerotic plaques and isolated macrophages from ApoE?/? mice fed a diet supplemented with the GSK3?/? inhibitor valproate had reduced levels of C/EBP homologous protein (CHOP). GSK3?/? inhibition blocked ER stress-induced lipid accumulation and the upregulation of genes associated with lipid metabolism. In primary mouse macrophages, PERK inhibition blocked ER stress-induced lipid accumulation, whereas constitutively active S9A-GSK3? promoted foam cell formation and CHOP expression, even in cells treated with a PERK inhibitor. These findings suggest that ER stress-PERK-GSK3?/? signaling promotes proatherogenic macrophage lipid accumulation. Twit Text FOAVip Protein kinase R-like endoplasmic reticulum kinase and glycogen synthase kinase-3 / regulate foam cell formation S ????J Lipid Res http://www.kidney.de/pget.php?&tw=1&pmid=25183803 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25183803 #FOAvip English Wikipedia <ref>{{Cite pmid|25183803}}</ref> Protein kinase R-like endoplasmic reticulum kinase and glycogen synthase kinase-3?/? regulate foam cell formation S #MMPMID25183803 McAlpine CS; Werstuck GH J Lipid Res 2014[Nov]; 55 (11): 2320-33 PMID25183803show ga Evidence suggests a causative role for endoplasmic reticulum (ER) stress in the development of atherosclerosis. This study investigated the potential role of glycogen synthase kinase (GSK)-3?/? in proatherogenic ER stress signaling. Thp1-derived macrophages were treated with the ER stress-inducing agents, glucosamine, thapsigargin, or palmitate. Using small-molecule inhibitors of specific unfolded protein response (UPR) signaling pathways, we found that protein kinase R-like ER kinase (PERK), but not inositol requiring enzyme 1 or activating transcription factor 6, is required for the activation of GSK3?/? by ER stress. GSK3?/? inhibition or siRNA-directed knockdown attenuated ER stress-induced expression of distal components of the PERK pathway. Macrophage foam cells within atherosclerotic plaques and isolated macrophages from ApoE?/? mice fed a diet supplemented with the GSK3?/? inhibitor valproate had reduced levels of C/EBP homologous protein (CHOP). GSK3?/? inhibition blocked ER stress-induced lipid accumulation and the upregulation of genes associated with lipid metabolism. In primary mouse macrophages, PERK inhibition blocked ER stress-induced lipid accumulation, whereas constitutively active S9A-GSK3? promoted foam cell formation and CHOP expression, even in cells treated with a PERK inhibitor. These findings suggest that ER stress-PERK-GSK3?/? signaling promotes proatherogenic macrophage lipid accumulation. äProtein kinase R-like endoplasmic reticulum kinase and glycogen syntha(epmc).pdf DeepDyve Pubget Overpricing