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Wang, Shiyu; Chen, Zhouji; Lam, Vivian; Han, Jaeseok; Hassler, Justin; Finck, Brian N.; Davidson, Nicholas O.; Kaufman, Randal J.
Cell metabolism, 10/2012, Letnik: 16, Številka: 4Journal Article
The unfolded protein response (UPR) is a signaling pathway required to maintain endoplasmic reticulum (ER) homeostasis and hepatic lipid metabolism. Here, we identify an essential role for the inositol-requiring transmembrane kinase/endoribonuclease 1α (IRE1α)-X box binding protein 1 (XBP1) arm of the UPR in regulation of hepatic very low-density lipoprotein (VLDL) assembly and secretion. Hepatocyte-specific deletion of Ire1α reduces lipid partitioning into the ER lumen and impairs the assembly of triglyceride (TG)-rich VLDL but does not affect TG synthesis, de novo lipogenesis, or the synthesis or secretion of apolipoprotein B (apoB). The defect in VLDL assembly is, at least in part, due to decreased microsomal triglyceride-transfer protein (MTP) activity resulting from reduced protein disulfide isomerase (PDI) expression. Collectively, our findings reveal a key role for the IRE1α-XBP1s-PDI axis in linking ER homeostasis with regulation of VLDL production and hepatic lipid homeostasis that may provide a therapeutic target for disorders of lipid metabolism. Display omitted ► Ire1α deletion impairs hepatic VLDL assembly, but not lipogenesis or apoB secretion ► IRE1α-XBP1s regulates TG partitioning into the smooth ER for VLDL assembly ► Inactivation of IRE1α in hepatocytes reduces PDI expression and MTP activity ► PDI restores MTP function and promotes VLDL secretion in Ire1α-deleted hepatocytes
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Leto | Faktor vpliva | Izdaja | Kategorija | Razvrstitev | ||||
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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