anti-MLX Interacting Protein (MLXIP) Antikörper

Human MLX Interacting Protein (MLXIP) Interaktionspartner

1. 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 (zeige TXNIP Antikörper)).

2. MondoA-directed programs have a key role in the coordinated control of myocyte lipid balance and insulin (zeige INS Antikörper) signaling

3. Evaluation of the conservation of ChREBP (zeige MLXIPL Antikörper) and MondoA sequences demonstrate that MondoA is better conserved and potentially mediates more ancient function in glucose metabolism.

4. These results suggest that C771G polymorphism of MLXIPL (zeige MLXIPL Antikörper) gene is associated with coronary stenosis and its severity.

5. Knockdown of MondoA, or its dimerization partner Mlx (zeige MLX Antikörper), blocks Myc (zeige MYC Antikörper)-induced reprogramming of multiple metabolic pathways, resulting in apoptosis

6. regulatory relationship between mTOR (zeige FRAP1 Antikörper) and the MondoA-TXNIP (zeige TXNIP Antikörper) axis that we propose contributes to glucose homeostasis

7. Suppression of Txnip (zeige TXNIP Antikörper) by lipopolysaccharide is accompanied by a decrease of the glucose sensing transcription factor MondoA in the nuclei.

8. An important contribution of MondoA to leukemia aggressiveness, which makes MondoA a potential candidate for targeted treatment of acute lymphoblastic leukemia.

9. the MondoA-TXNIP (zeige TXNIP Antikörper) regulatory circuit has a role in the hexose transport curb, although other redundant pathways also contribute

10. Induction of TXNIP (zeige TXNIP Antikörper) 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.

Mouse (Murine) MLX Interacting Protein (MLXIP) Interaktionspartner

1. 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 (zeige TXNIP Antikörper)).

2. MondoA-directed programs have a key role in the coordinated control of myocyte lipid balance and insulin (zeige INS Antikörper) signaling

3. Evaluation of the conservation of ChREBP (zeige MLXIPL Antikörper) and MondoA sequences demonstrate that MondoA is better conserved and potentially mediates more ancient function in glucose metabolism.

4. MondoA is a basic helix-loop-helix/leucine zipper transcription factor (zeige NRL Antikörper) that is expressed predominantly in skeletal muscle. Mice deficient for MondoA excel in sprinting, as their skeletal muscles display an enhanced glycolytic capacity.

5. MondoA-Mlx (zeige MLX Antikörper) complexes sense elevated levels of G6P and adenine nucleotides to trigger a TXNIP (zeige TXNIP Antikörper)-dependent feedback inhibition of glycolysis

6. Suppression of Txnip (zeige TXNIP Antikörper) by lipopolysaccharide is accompanied by a decrease of the glucose sensing transcription factor MondoA in the nuclei.

7. the MondoA-TXNIP (zeige TXNIP Antikörper) regulatory circuit has a role in the hexose transport curb, although other redundant pathways also contribute

8. Induction of TXNIP (zeige TXNIP Antikörper) 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.