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).

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

3. Evaluation of the conservation of ChREBP 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 gene is associated with coronary stenosis and its severity.

5. Knockdown of MondoA, or its dimerization partner Mlx, blocks Myc-induced reprogramming of multiple metabolic pathways, resulting in apoptosis

6. regulatory relationship between mTOR and the MondoA-TXNIP axis that we propose contributes to glucose homeostasis

7. Suppression of Txnip 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 regulatory circuit has a role in the hexose transport curb, although other redundant pathways also contribute

10. Induction of TXNIP 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.

11. Glucose is required at two additional steps to stimulate the transcription activation function of MondoA-Mlx complexes.

12. Data show that for both MondoA and Mlx, the C-terminal domain CRM-1 has cytoplasmic localization activity that is required by the protein monomers to accumulate in the cytoplasm.

13. Endogenous MondoA and Mlx associate with mitochondria in primary skeletal muscle.

14. These studies suggest a key role for MondoA:Mlx complexes in the adaptive transcriptional response to changes in extracellular glucose concentration and peripheral glucose uptake.

15. Data suggest that glutamine-dependent mitochondrial anapleurosis dictates glucose uptake and aerobic glycolysis by blocking MondoA:Mlx-dependent transcriptional activation of TXNIP.

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).

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

3. Evaluation of the conservation of ChREBP 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 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 complexes sense elevated levels of G6P and adenine nucleotides to trigger a TXNIP-dependent feedback inhibition of glycolysis

6. Suppression of Txnip by lipopolysaccharide is accompanied by a decrease of the glucose sensing transcription factor MondoA in the nuclei.

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

8. Induction of TXNIP 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.