Regulation of mouse sterol regulatory element-binding protein-1c gene (SREBP-1c) by oxysterol receptors, LXRalpha and LXRbeta.

By J. Repa, G. Liang, J. Ou, Y. Bashmakov, J. Lobaccaro, I. Shimomura, B. Shan, M. Brown, J. Goldstein, D. Mangelsdorf. Genes & Development, 2000

814 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/88f3368b86751226ea93373db0cfc665b612b8e9

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Citations in the corpus

Molecular mechanism of PPARα action and its impact on lipid metabolism, inflammation and fibrosis in non-alcoholic fatty liver disease. (2015, unknown): “Journal of Hepatology 201 transcriptional activity [95,100].”
SREBP Activity Is Regulated by mTORC1 and Contributes to Akt-Dependent Cell Growth (2008, background): “The observed induction of flSREBP in response to sterol treatment is most likely due to activation of the liver X receptor (LXR) (Repa et al., 2000) (Figure 2F).”
INFLAMMATION AND LIPID SIGNALING IN THE ETIOLOGY OF INSULIN RESISTANCE (2012, unknown): “Liver X receptors induce expression of SREBP1c, as well as directly regulate numerous genes involved in fatty acid biosynthesis and metabolism (Repa et al., 2000; Schultz et al., 2000).”
Enzymes of triacylglycerol synthesis and their regulation. (2004, background): “The SREBP-1c promoter contains an LXR binding site [219], and mice lacking LXRa and b express less SREBP-1c and its target liver genes [220].”
Hepatic steatosis: a role for de novo lipogenesis and the transcription factor SREBP‐1c (2010, background): “In contrast, animals fed on a high-cholesterol diet or synthetic LXR agonists show a selective increase in SREBP-1c mRNA and nuclear protein, induced expression of lipogenic target genes and elevated rates of lipogenesis [34,35].”
Liver-specific disruption of PPARgamma in leptin-deficient mice improves fatty liver but aggravates diabetic phenotypes. (2003, background): “Furthermore, SREBP1c expression is markedly increased in an LXR-dependent manner (42, 43).”
Regulation of energy metabolism by long-chain fatty acids. (2014, background): “In liver of rodents, PUFAs suppress expression and activity of SREBP1c and ChREBP, key transcription factors to induce genes for de novo lipogenesis.”
Bile Acid Signaling in Metabolic Disease and Drug Therapy (2014, background): “Insulin is known to induce both SREBP-1c mRNA expression by the liver orphan receptor (LXR) and proteolytic cleavage (Repa et al., 2000; Shao and Espenshade, 2012).”
Hepatic fatty acid transporter Cd36 is a common target of LXR, PXR, and PPARgamma in promoting steatosis. (2008, background): “As summarized in Figure 7, PPAR may conribute to the regulation of Cd36 by (1) direct transcripional regulation,25 (2) being activated by PXR (this tudy), and (3) being activated by LXR46 (Figure 7).”