Disease relevance of Nr1h3

• In conclusion, hypercholesterolemia in McA-RH7777 hepatoma-bearing rats was caused by increased cholesterol efflux from tumors as a result of activation of LXRalpha [1].

High impact information on Nr1h3

• In contrast, a DR-4-dependent constitutive transcriptional activation of a chloramphenicol acetyltransferase reporter gene by the RLD-1/RXR alpha heterodimer was observed [2].
• RLD-1 preferentially binds as a heterodimer with RXR to a direct repeat of the half-site sequence 5'-G/AGGTCA-3', separated by four nucleotides (DR-4) [2].
• Comparative analysis of quiescent and activated HSC in culture reveals higher expression of putative adipogenic transcription factors such as CCAAT/enhancer-binding protein (C/EBP) alpha, C/EBPbeta, C/EBPdelta, PPARgamma, liver X receptor alpha, sterol regulatory element-binding protein 1c and of adipocyte-specific genes in the quiescent cells [3].
• The role of liver X receptor-alpha in the fatty acid regulation of hepatic gene expression [4].
• Finally, peroxisome proliferator-activated receptor-alpha and -delta and liver X receptor-alpha and -beta mRNAs were detected in fetal epidermis by reverse transcriptase-polymerase chain reaction and northern analyses [5].

Biological context of Nr1h3

• As LXRalpha regulates expression of sterol response element binding protein-1c (SREBP-1c) expression, we measured SREBP-1c expression [6].
• In conclusion, changes in liver cholesterol and TG concentrations in Fe-restricted fetuses may be coordinated through reduced expression of heme-containing cholesterol 7alpha hydroxylase and its regulator LXRalpha, mainly via downregulation of expression of genes in bile acid synthesis and fatty acid synthesis pathways [6].
• Liver X receptor alpha (LXRalpha) and liver X receptor beta(LXRbeta are oxysterol receptors that regulate multiple target genes involved in cholesterol homeostasis [7].

Anatomical context of Nr1h3

• This regulation is not a direct effect of GH on hepatocytes and does not involve changed expression of SREBP-1c or LXRalpha mRNA but is associated with decreased insulin sensitivity [8].

Associations of Nr1h3 with chemical compounds

• In addition, bile acid biosynthesis was inhibited despite the reduced expression of the small heterodimer partner (SHP) and activated LXRalpha, which also appeared to contribute to the accumulation of oxysterols followed by the acceleration of cholesterol efflux [1].
• Oxysterols are potent regulators of the activities of transcription factors of the sterol regulatory element-binding protein family and of liver X-receptor alpha [9].
• Although gemfibrozil induced mild effects on hepatic PPARalpha, HNF-4, and LXRalpha, only rosiglitazone significantly reduced plasma TG (59%), glucose (19%), insulin (61%), and leptin (66%), and liver TG (43%), CE (49%), and NEFA (27%) [10].
• Clofibrate also enhanced the expression of mRNAs for PPARalpha, LXRalpha, and ABCA1 [11].
• Clofibrate increased the levels of liver microsomal oxysterols including 25- and 27-hydroxycholesterol, which are potent activators of LXRalpha [11].

Analytical, diagnostic and therapeutic context of Nr1h3

• The levels of mRNAs for liver X receptor alpha (LXRalpha), ATP-binding cassette A1 (ABCA1), PPARalpha and cholesterol 7alpha-hydroxylase (CYP7A) in the liver were analyzed by northern blotting [11].

References