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anti-Human MLXIPL Antibodies:
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Human Polyclonal MLXIPL Primary Antibody for 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
Show all 89 Pubmed References
Human Polyclonal MLXIPL Primary Antibody for 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
Show all 6 Pubmed References
Polyclonal MLXIPL Primary Antibody for 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
Show all 3 Pubmed References
Human Polyclonal MLXIPL Primary Antibody for 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
Show all 2 Pubmed References
Human Monoclonal MLXIPL Primary Antibody for 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
Show all 2 Pubmed References
Human Polyclonal MLXIPL Primary Antibody for 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
A nutrient-sensitive mTOR (show FRAP1 Antibodies)/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 Antibodies) resistance.
results indicated that the age and total cholesterol concentrations were independent influential factors of ChREBP methylation and DNMT1 (show DNMT1 Antibodies) variants could probably influence LDL-C to further modify ChREBP DNA methylation (show HELLS Antibodies)
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 Antibodies) 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 Antibodies) promoted ChREBP transcription in response to glucose, and also demonstrated that ChREBP-alpha and HNF-4alpha (show HNF4A Antibodies) synergistically increased ChREBP-beta transcription.
High glucose-mediated induction of PDGF-C (show PDGFC Antibodies) 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 Antibodies) sequences demonstrate that MondoA (show MLXIP Antibodies) is better conserved and potentially mediates more ancient function in glucose metabolism.
Metformin down-regulates high-glucose-induced TXNIP (show TXNIP Antibodies) transcription by inactivating ChREBP and FOXO1 (show FOXO1 Antibodies) in endothelial cells, partially through AMP-activated protein kinase (show PRKAA2 Antibodies) activation
Data suggest that triiodothyronine and high glucose signal coordinately to up-regulate ChREBP, Ucp1 (show UCP1 Antibodies), Glut4 (show SLC2A4 Antibodies), and Fasn (show FASN Antibodies) 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 Antibodies) = uncoupling protein-1 (show UCP1 Antibodies); Glut4 (show SLC2A4 Antibodies) = facilitated glucose transporter (show SLC2A12 Antibodies)-4; Fasn (show FASN Antibodies) = fatty acid synthase (show FASN Antibodies), 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 Antibodies)-dependent cholesterol metabolism.
a high complex carbohydrate diet selectively increases hepatic ChREBPbeta expression, which associates with hepatic steatosis but not insulin (show INS Antibodies) resistance. In contrast, a high fat diet reduces adipose ChREBP, which associates with inflammation and insulin (show INS Antibodies) resistance.
the synergistic action of ChREBP and SREBP-1c (show SREBF1 Antibodies) is necessary for the maximal induction of Elovl6 (show ELOVL6 Antibodies) expression in the liver.
Adipose tissue mTORC2 (show CRTC2 Antibodies) regulates via Rictor (show RICTOR Antibodies) ChREBP-driven de novo lipogenesis and hepatic glucose metabolism.
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