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ChREBP was initially studied as a master regulator of lipogenesis in liver and fat tissue, it is now clear that ChREBP functions as a central metabolic coordinator in a variety of cell types in response to environmental and hormonal signals, with wide implications in health and disease.
A nutrient-sensitive mTOR (show FRAP1 Proteins)/ChREBP regulated transcriptional network could be a novel target to improve beta cell survival and glucose homeostasis in diabetes.
these findings support a carbohydrate-mediated, ChREBP-driven mechanism that contributes to hepatic insulin (show INS Proteins) resistance.
results indicated that the age and total cholesterol concentrations were independent influential factors of ChREBP methylation and DNMT1 (show DNMT1 Proteins) variants could probably influence LDL-C to further modify ChREBP DNA methylation (show HELLS Proteins)
p = 6.69 x 10(-9) ] on chr7 at the carbohydrate-responsive element-binding protein-encoding (MLXIPL) gene locus displayed significant protective characteristics, while another variant rs6982502 [0.76 (0.68-0.84); p = 5.31 x 10(-7) ] on chr8 showed similar but weaker properties.
ChREBP role in non-alcoholic fatty liver disease.The involvement of ChREBP in FASN (show FASN Proteins) promoter histone modification.
This cross-sectional study suggests that MLXIPL rs3812316 genotypes may be associated with Triglyceride levels. there were significantly different genotype distributions in two TG categories: (1) subjects with normal TG values had a significantly higher G allele frequency than those with elevated TG levels
The results revealed the novel mechanism by which HNF-4alpha (show HNF4A Proteins) promoted ChREBP transcription in response to glucose, and also demonstrated that ChREBP-alpha and HNF-4alpha (show HNF4A Proteins) synergistically increased ChREBP-beta transcription.
High glucose-mediated induction of PDGF-C (show PDGFC Proteins) via ChREBP in mesangial cells contributes to the development of glomerular mesangial expansion in diabetes.
Evaluation of the conservation of ChREBP and MondoA (show MLXIP Proteins) sequences demonstrate that MondoA (show MLXIP Proteins) is better conserved and potentially mediates more ancient function in glucose metabolism.
Study identify O-GlcNAcylation on Ser514 in the C-terminus of ChREBP and validate two important sites, Thr517 and Ser839 for O-GlcNAcylation and their function. Ser514 phosphorylation enhances ChREBP O-GlcNAcylation, maintaining the transcriptional activity of ChREBP; Ser839 O-GlcNAcylation is essential for its heterodimerization, DNA-binding activity, and nuclear export.
Data suggest that triiodothyronine and high glucose signal coordinately to up-regulate ChREBP, Ucp1 (show UCP1 Proteins), Glut4 (show SLC2A4 Proteins), and Fasn (show FASN Proteins) in brown adipocytes; ChREBP plays role as a central regulator of brown adipocyte activity/energy metabolism. (ChREBP = carbohydrate-responsive element-binding protein; Ucp1 (show UCP1 Proteins) = uncoupling protein-1 (show UCP1 Proteins); Glut4 (show SLC2A4 Proteins) = facilitated glucose transporter (show SLC2A12 Proteins)-4; Fasn (show FASN Proteins) = fatty acid synthase (show FASN Proteins), type-I)
findings suggest that a previously unknown link exists between ChREBP and the regulation of cholesterol synthesis that affects liver injury.
findings also identified a role for ChREBP in regulating SREBP2 (show SREBF2 Proteins)-dependent cholesterol metabolism.
a high complex carbohydrate diet selectively increases hepatic ChREBPbeta expression, which associates with hepatic steatosis but not insulin (show INS Proteins) resistance. In contrast, a high fat diet reduces adipose ChREBP, which associates with inflammation and insulin (show INS Proteins) resistance.
the synergistic action of ChREBP and SREBP-1c is necessary for the maximal induction of Elovl6 expression in the liver.
This gene encodes a basic helix-loop-helix leucine zipper transcription factor of the Myc/Max/Mad superfamily. This protein forms a heterodimeric complex and binds and activates, in a glucose-dependent manner, carbohydrate response element (ChoRE) motifs in the promoters of triglyceride synthesis genes. The gene is deleted in Williams-Beuren syndrome, a multisystem developmental disorder caused by the deletion of contiguous genes at chromosome 7q11.23.
MLX interacting protein-like
, carbohydrate response element binding protein variant 1
, carbohydrate response element binding protein variant 2
, Williams-Beuren syndrome chromosomal region 14 protein homolog
, carbohydrate responsive element binding protein
, williams-Beuren syndrome chromosomal region 14 protein homolog
, MLX-interacting protein-like
, Mlx interactor
, WS basic-helix-loop-helix leucine zipper protein
, Williams Beuren syndrome chromosome region 14
, Williams-Beuren syndrome chromosome region 14 protein 1
, Williams-Beuren syndrome chromosome region 14 protein 2
, carbohydrate response element binding protein
, carbohydrate-responsive element-binding protein
, class D basic helix-loop-helix protein 14
, williams-Beuren syndrome chromosomal region 14 protein
, MLX interacting protein-like beta
, MLX interactor
, Williams-Beuren syndrome chromosome region 14 homolog
, putative hepatic transcription factor
, WBSCR14 protein-like
, Williams-Beuren syndrome chromosomal region 14 protein