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MONDOA forms heterodimers with MLX (MIM 602976) that can bind to and activate transcription from CACGTG E boxes (Billin et al., 2000 [PubMed 11073985]).[supplied by OMIM, Mar 2008].. Additionally we are shipping MLX Interacting Protein Antibodies (38) and MLX Interacting Protein Kits (4) and many more products for this protein.
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Data (including data from studies in knockout mice) suggest that MONDOA shuttles to nucleus of pancreatic beta-cells where it is required for induction of glucose-responsive genes arrestin domain-containing protein 4 (ARRDC4) and thioredoxin interacting protein (TXNIP (show TXNIP Proteins)).
MondoA-directed programs have a key role in the coordinated control of myocyte lipid balance and insulin (show INS Proteins) signaling
Evaluation of the conservation of ChREBP (show MLXIPL Proteins) and MondoA sequences demonstrate that MondoA is better conserved and potentially mediates more ancient function in glucose metabolism.
These results suggest that C771G polymorphism of MLXIPL (show MLXIPL Proteins) gene is associated with coronary stenosis and its severity.
Knockdown of MondoA, or its dimerization partner Mlx (show MLX Proteins), blocks Myc (show MYC Proteins)-induced reprogramming of multiple metabolic pathways, resulting in apoptosis
regulatory relationship between mTOR (show FRAP1 Proteins) and the MondoA-TXNIP (show TXNIP Proteins) axis that we propose contributes to glucose homeostasis
Suppression of Txnip (show TXNIP Proteins) by lipopolysaccharide is accompanied by a decrease of the glucose sensing transcription factor MondoA in the nuclei.
An important contribution of MondoA to leukemia aggressiveness, which makes MondoA a potential candidate for targeted treatment of acute lymphoblastic leukemia.
the MondoA-TXNIP (show TXNIP Proteins) regulatory circuit has a role in the hexose transport curb, although other redundant pathways also contribute
Induction of TXNIP (show TXNIP Proteins) under lactic acidosis is caused by the activation of the glucose-sensing helix-loop-helix transcriptional complex MondoA:Mlx, which is usually triggered upon glucose exposure.
Data (including data from studies in knockout mice) suggest that MondoA shuttles to nucleus of pancreatic beta-cells where it is required for induction of glucose-responsive genes arrestin domain-containing protein 4 (Arrdc4) and thioredoxin interacting protein (Txnip (show TXNIP Proteins)).
MondoA is a basic helix-loop-helix/leucine zipper transcription factor (show NRL Proteins) that is expressed predominantly in skeletal muscle. Mice deficient for MondoA excel in sprinting, as their skeletal muscles display an enhanced glycolytic capacity.
MondoA-Mlx (show MLX Proteins) complexes sense elevated levels of G6P and adenine nucleotides to trigger a TXNIP (show TXNIP Proteins)-dependent feedback inhibition of glycolysis
MONDOA forms heterodimers with MLX (MIM 602976) that can bind to and activate transcription from CACGTG E boxes (Billin et al., 2000
MLX interacting protein
, MLX-interacting protein-like
, MLX-interacting protein
, Mlx interactor
, class E basic helix-loop-helix protein 36
, transcriptional activator MondoA