Phosphotyrosine Interaction Domain Containing 1 Proteins (PID1)

Human Phosphotyrosine Interaction Domain Containing 1 (PID1) interaction partners

1. Overall survival and radiation-free progression-free survival were longer in medulloblastoma patients whose tumors had higher PID1 mRNA levels.

2. overexpression of TFAM can restore mitochondrial function to normal levels in NYGGF4-overexpressing adipocytes

3. NYGGF4 plays a role in IR and its effects on IR could be reversed by metformin through activating IRS-1/PI3K/Akt and AMPK-PGC1-alpha pathways.

4. NYGGF4 acts directly on the IRS1/PI3K/AKT insulin pathway to reduce glucose uptake and transport, impairs mitochondrial function and causes insulin resistance, and thus may be a useful therapeutic target for obesity-associated insulin resistance.

5. Overexpression of NYGGF4 caused mitochondrial dysfunction in adipocytes, which might be responsible for the development of NYGGF4-induced insulin resistance.

6. TNFA up-regulated the expression of NYGGF4 during preadipocyte differentiation.

7. NYGGF4 over-expression impairs the insulin sensitivity of 3T3-L1 adipocytes through decreasing GLUT4 translocation and had no effects on the secretory function of adipocytes.

8. A novel gene named NYGGF4, which was expressed at a higher level in obese subjects, was isolated and characterized and could play a role in cell growth and adipogenesis process

9. Data show that NYGGF4 regulates the functions of IRS-1 and Akt, decreases GLUT4 translocation and reduces glucose uptake in response to insulin.

10. Q7Z2X4 protein (PID1) identified as a cytosolic ligand of LRP1 in a trimeric complex with Cubilin. Q7Z2X4 named PCLI1 (PTB-containing, Cubilin and LRP1 Interacting protein 1)

Mouse (Murine) Phosphotyrosine Interaction Domain Containing 1 (PID1) interaction partners

1. Results thus indicate phosphotyrosine interaction domain containing 1 (PID1) as a critical regulator of glucose metabolism in adipocytes.

2. data demonstrate that differentially methylated genes are significantly overrepresented in NYGGF4-overexpression adipocytes, providing valuable clues for further exploration of the role of NYGGF4 in insulin sensitivity regulation.

3. These results suggested that addition of silencing NYGGF4 partly rescued the effect of insulin resistance and mitochondrial dysfunction in NYGGF4 silenced 3T3-L1 adipocytes incubated with cyanide p-trifluoromethoxyphenyl-hydrazone.

4. Data demonstrate that NYGGF4 knockdown increases glucose transport in myocytes by activation of the IRS-1/PI3K/AKT insulin pathway.

5. Lipoic acid protects 3T3-L1 adipocytes from NYGGF4-induced IR partially through increasing phosphorylation of IRS-1 and Akt

6. NYGGF4 reduced intracellular ATP concentration and promoted an increase in mitochondrial transmembrane potential and reactive oxygen species level without affecting mitochondrial morphology or mtDNA.

7. The expression of NYGGF4 mRNA is affected by a variety of factors that are related to insulin sensitivity.[NYGGF4]