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Human Polyclonal MLXIPL Primary Antibody für ChIP, ICC - ABIN152902
Wang, Botolin, Xu, Christian, Mitchell, Jayaprakasam, Nair, Nair, Peters, Peters, Busik, Busik, Olson, Jump: Regulation of hepatic fatty acid elongase and desaturase expression in diabetes and obesity. in Journal of lipid research 2006
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Human Polyclonal MLXIPL Primary Antibody für ICC, IF - ABIN152903
Proszkowiec-Weglarz, Humphrey, Richards: Molecular cloning and expression of chicken carbohydrate response element binding protein and Max-like protein X gene homologues. in Molecular and cellular biochemistry 2008
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Polyclonal MLXIPL Primary Antibody für IF, WB - ABIN540822
Letexier, Pinteur, Large, Fréring, Beylot: Comparison of the expression and activity of the lipogenic pathway in human and rat adipose tissue. in Journal of lipid research 2003
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Human Monoclonal MLXIPL Primary Antibody für ICC, ELISA - ABIN1724913
Hurtado del Pozo, Vesperinas-García, Rubio, Corripio-Sánchez, Torres-García, Obregon, Calvo: ChREBP expression in the liver, adipose tissue and differentiated preadipocytes in human obesity. in Biochimica et biophysica acta 2011
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Human Polyclonal MLXIPL Primary Antibody für IHC, IHC (p) - ABIN446286
Butcher, Torrecilla, Young, Kong, Mistry, Bottrill, Tobin: N-methyl-D-aspartate receptors mediate the phosphorylation and desensitization of muscarinic receptors in cerebellar granule neurons. in The Journal of biological chemistry 2009
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Human Polyclonal MLXIPL Primary Antibody für ICC, IF - ABIN4298323
Kaushik, Shojaie, Panzitt, Sonavane, Venghatakrishnan, Manikkam, Zaslavsky, Putluri, Vasu, Zhang, Khan, Lloyd, Szafran, Dasgupta, Bader, Stossi, Li, Samanta, Cao, Tsouko, Huang, Frigo, Chan, Edwards et al.: Inhibition of the hexosamine biosynthetic pathway promotes castration-resistant prostate cancer. ... in Nature communications 2016
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 (zeige FRAP1 Antikörper)/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 (zeige INS Antikörper) resistance.
results indicated that the age and total cholesterol concentrations were independent influential factors of ChREBP methylation and DNMT1 (zeige DNMT1 Antikörper) variants could probably influence LDL-C to further modify ChREBP DNA methylation (zeige HELLS Antikörper)
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 (zeige FASN Antikörper) 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 (zeige HNF4A Antikörper) promoted ChREBP transcription in response to glucose, and also demonstrated that ChREBP-alpha and HNF-4alpha (zeige HNF4A Antikörper) synergistically increased ChREBP-beta transcription.
High glucose-mediated induction of PDGF-C (zeige PDGFC Antikörper) via ChREBP in mesangial cells contributes to the development of glomerular mesangial expansion in diabetes.
Evaluation of the conservation of ChREBP and MondoA (zeige MLXIP Antikörper) sequences demonstrate that MondoA (zeige MLXIP Antikörper) is better conserved and potentially mediates more ancient function in glucose metabolism.
loss of adipose-ChREBP is sufficient to cause insulin (zeige INS Antikörper) resistance potentially by regulating AT glucose transport.
Glucose-challenged Chrebp-/- mice exhibit a marked reduction in FGF21 (zeige FGF21 Antikörper) production.
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 (zeige UCP1 Antikörper), Glut4 (zeige SLC2A4 Antikörper), and Fasn (zeige FASN Antikörper) in brown adipocytes; ChREBP plays role as a central regulator of brown adipocyte activity/energy metabolism. (ChREBP = carbohydrate-responsive element-binding protein; Ucp1 (zeige UCP1 Antikörper) = uncoupling protein-1 (zeige UCP1 Antikörper); Glut4 (zeige SLC2A4 Antikörper) = facilitated glucose transporter (zeige SLC2A12 Antikörper)-4; Fasn (zeige FASN Antikörper) = fatty acid synthase (zeige FASN Antikörper), 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 (zeige SREBF2 Antikörper)-dependent cholesterol metabolism.
a high complex carbohydrate diet selectively increases hepatic ChREBPbeta expression, which associates with hepatic steatosis but not insulin (zeige INS Antikörper) resistance. In contrast, a high fat diet reduces adipose ChREBP, which associates with inflammation and insulin (zeige INS Antikörper) resistance.
the synergistic action of ChREBP and SREBP-1c (zeige SREBF1 Antikörper) is necessary for the maximal induction of Elovl6 (zeige ELOVL6 Antikörper) 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