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Increases proliferation of preadipocytes without affecting adipocytic differentiation (By similarity).. Additionally we are shipping PID1 Antibodies (33) and PID1 Kits (4) and many more products for this protein.
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Overall survival and radiation-free progression-free survival were longer in medulloblastoma patients whose tumors had higher PID1 mRNA levels.
Pid1 is a potent intracellular inhibitor of insulin (show INS Proteins) signaling pathway during obesity in humans and mice.
overexpression of TFAM (show TFAM Proteins) can restore mitochondrial function to normal levels in NYGGF4-overexpressing adipocytes
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.
NYGGF4 acts directly on the IRS1 (show IRS1 Proteins)/PI3K (show PIK3CA Proteins)/AKT (show AKT1 Proteins) insulin (show INS Proteins) pathway to reduce glucose uptake and transport, impairs mitochondrial function and causes insulin (show INS Proteins) resistance, and thus may be a useful therapeutic target for obesity-associated insulin (show INS Proteins) resistance.
Overexpression of NYGGF4 caused mitochondrial dysfunction in adipocytes, which might be responsible for the development of NYGGF4-induced insulin (show INS Proteins) resistance.
TNFA (show TNF Proteins) up-regulated the expression of NYGGF4 during preadipocyte differentiation.
NYGGF4 over-expression impairs the insulin (show INS Proteins) sensitivity of 3T3-L1 adipocytes through decreasing GLUT4 (show SLC2A4 Proteins) translocation and had no effects on the secretory function of adipocytes.
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
Data show that NYGGF4 regulates the functions of IRS-1 (show IRS1 Proteins) and Akt (show AKT1 Proteins), decreases GLUT4 (show SLC2A4 Proteins) translocation and reduces glucose uptake in response to insulin (show INS Proteins).
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 (show INS Proteins) sensitivity regulation.
These results suggested that addition of silencing NYGGF4 partly rescued the effect of insulin (show INS Proteins) resistance and mitochondrial dysfunction in NYGGF4 silenced 3T3-L1 adipocytes incubated with cyanide p-trifluoromethoxyphenyl-hydrazone.
Data demonstrate that NYGGF4 knockdown increases glucose transport in myocytes by activation of the IRS-1 (show IRS1 Proteins)/PI3K/AKT (show AKT1 Proteins) insulin (show INS Proteins) pathway.
Lipoic acid protects 3T3-L1 adipocytes from NYGGF4-induced IR partially through increasing phosphorylation of IRS-1 (show IRS1 Proteins) and Akt (show AKT1 Proteins)
NYGGF4 reduced intracellular ATP concentration and promoted an increase in mitochondrial transmembrane potential and reactive oxygen species level without affecting mitochondrial morphology or mtDNA.
The expression of NYGGF4 mRNA is affected by a variety of factors that are related to insulin (show INS Proteins) sensitivity.[NYGGF4]
Increases proliferation of preadipocytes without affecting adipocytic differentiation (By similarity).
PTB-containing, cubilin and LRP1-interacting protein
, phosphotyrosine interaction domain-containing protein 1
, NYGGF4-like protein