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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. Additionally we are shipping MLX Interacting Protein Kits (4) and MLX Interacting Protein Proteins (4) and many more products for this protein.
Showing 10 out of 38 products:
Cow (Bovine) Polyclonal MLXIP Primary Antibody for WB - ABIN610684
Das, Lewis, Scherer, Lisanti: The membrane-spanning domains of caveolins-1 and -2 mediate the formation of caveolin hetero-oligomers. Implications for the assembly of caveolae membranes in vivo. in The Journal of biological chemistry 1999
Show all 3 Pubmed References
Dog (Canine) Polyclonal MLXIP Primary Antibody for IHC, WB - ABIN2776519
Stoltzman, Peterson, Breen, Muoio, Billin, Ayer: Glucose sensing by MondoA:Mlx complexes: a role for hexokinases and direct regulation of thioredoxin-interacting protein expression. in Proceedings of the National Academy of Sciences of the United States of America 2008
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 Antibodies)).
MondoA-directed programs have a key role in the coordinated control of myocyte lipid balance and insulin (show INS Antibodies) signaling
Evaluation of the conservation of ChREBP (show MLXIPL Antibodies) 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 Antibodies) gene is associated with coronary stenosis and its severity.
Knockdown of MondoA, or its dimerization partner Mlx (show MLX Antibodies), blocks Myc (show MYC Antibodies)-induced reprogramming of multiple metabolic pathways, resulting in apoptosis
regulatory relationship between mTOR (show FRAP1 Antibodies) and the MondoA-TXNIP (show TXNIP Antibodies) axis that we propose contributes to glucose homeostasis
Suppression of Txnip (show TXNIP Antibodies) 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 Antibodies) regulatory circuit has a role in the hexose transport curb, although other redundant pathways also contribute
Induction of TXNIP (show TXNIP Antibodies) 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 Antibodies)).
MondoA is a basic helix-loop-helix/leucine zipper transcription factor (show NRL Antibodies) 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 Antibodies) complexes sense elevated levels of G6P and adenine nucleotides to trigger a TXNIP (show TXNIP Antibodies)-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