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MLXIPL encodes a basic helix-loop-helix leucine zipper transcription factor of the Myc/Max/Mad superfamily. Additionally we are shipping MLXIPL Proteins (3) and many more products for this protein.
Showing 10 out of 113 products:
Human Polyclonal MLXIPL Primary Antibody for EIA, IHC (p) - ABIN953464
Johansen, Wang, Lanktree, Cao, McIntyre, Ban, Martins, Kennedy, Hassell, Visser, Schwartz, Voight, Elosua, Salomaa, ODonnell, Dallinga-Thie, Anand, Yusuf, Huff, Kathiresan, Hegele: Excess of rare variants in genes identified by genome-wide association study of hypertriglyceridemia. in Nature genetics 2010
Show all 4 references for ABIN953464
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 references for ABIN1724913
Cow (Bovine) Polyclonal MLXIPL Primary Antibody for IHC, WB - ABIN2778415
Cairo, Merla, Urbinati, Ballabio, Reymond: WBSCR14, a gene mapping to the Williams--Beuren syndrome deleted region, is a new member of the Mlx transcription factor network. in Human molecular genetics 2001
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
Polymorphisms in lipid level modifier MLXIPL, GCKR (show GCKR Antibodies), GALNT2 (show GALNT2 Antibodies), CILP2 (show Cilp2 Antibodies), ANGPTL3 (show ANGPTL3 Antibodies) and TRIB1 (show TRIB1 Antibodies) genes are highly associated with plasma lipid level changes.
Single-nucleotide polymorphisms alleles near MLXIPL that were associated with higher coffee consumption.
A major function of Mio in mitosis is to regulate the activation/deactivation of Plk1 (show PLK1 Antibodies) and Aurora A (show AURKA Antibodies).
the single nucleotide polymorphism of MLXIPL is significantly associated with Non-alcoholic Fatty Liver Disease.
results demonstrate that AGEs-RAGE (show AGER Antibodies) signaling enhances cancer cell proliferation in which AGEs-mediated ChREBP induction plays an important role.
Significant linkage disequilibria were noted among ZNF259 (show znf259 Antibodies), BUD13 and MLXIPL SNPs and serum lipid levels.
demonstrates that Chrebp interacts with AR and regulates its transcriptional activity
Adipose tissue mTORC2 (show CRTC2 Antibodies) regulates via Rictor (show RICTOR Antibodies) ChREBP-driven de novo lipogenesis and hepatic glucose metabolism.
Targeted deletion of ChREBP in bone marrow cells resulted in accelerated atherosclerosis progression in Ldlr (show LDLR Antibodies)-/- mice with increased monocytosis, lesional macrophage accumulation, and plaque necrosis.
Data show that carbohydrate-response element-binding protein (ChREBP) activation induces peroxisome proliferator-activated receptor (PPARgamma (show PPARG Antibodies)) activity and ChREBP inhibition impairs differentiation.
hyperinsulinemia may cause glycolipid metabolic disorders by up-regulating the expression of ChREBP
LXRs act as nutrient and glucose metabolic sensors upstream of ChREBP
The effects of ethanol on AMPK (show PRKAA1 Antibodies) and PP2A (show PPP2R2B Antibodies) may result in activation of ChREBP, providing another potential mechanism for ethanol-induced hepatic steatosis.
Depletion of ChREBP decreased glucose-stimulated proliferation in beta-cells isolated from ChREBP(-/-) mice, in INS-1-derived 832/13 cells, and in primary rat and human beta-cells
Data indicate that ChREBP is a key transcription factor that mediates many of the hyperglycaemia-induced activations in a gene expression programme that underlies beta cell glucotoxicity at the molecular, cellular and whole animal levels.
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