NR1H2 和 NR1H3 调节胆固醇摄取以限制
中文名称
通路描述
肝脏 X 受体 NR1H3 (LXR alpha) 和 NR1H2 (LXR beta) 是固醇响应转录因子，在与它们的相应氧化固醇配体结合时激活。配体激活的 NR1H2 和 NR1H3 诱导旨在通过限制胆固醇摄取、抑制胆固醇生物合成和促进胆固醇排出来减少细胞固醇负荷的遗传程序。此 Reactome 模块描述了 NR1H2 和 NR1H3 调节的 MYLIP (IDOL) 基因表达，这是一种 E3 泛素连接酶，触发 LDLR 的低密度脂蛋白受体 (LDLR) 的泛素化，将其靶向降解，从而限制胆固醇摄取 (Zelcer N et al. 2009; Zhang L et al. 2012)。
英文描述
NR1H2 & NR1H3 regulate gene expression to limit cholesterol uptake Liver X receptors NR1H3 (LXR alpha) and NR1H2 (LXR beta) are sterol-responsive transcription factors that become activated upon the engagement with their cognate oxysterol ligands. Ligand-activated NR1H2 & NR1H3 induce a genetic program aimed at reducing the cellular sterol load by limiting cholesterol uptake, attenuating cholesterol biosynthesis and promoting cholesterol efflux. This Reactome module describes the NR1H2 & NR1H3-regulated expression of MYLIP (IDOL) gene, an E3 ubiquitin ligase, that triggers ubiquitination of the low-density lipoprotein receptor (LDLR) on its cytoplasmic domain, targeting it for degradation and thereby limiting cholesterol uptake (Zelcer N et al. 2009; Zhang L et al. 2012).
所含基因
5 个基因