What IGF-1 inhibits?
Metabolic effects One important metabolic effect of IGF-1 is its ability to signal cells that sufficient nutrients are available for cells to undergo hypertrophy and cell division. These signals also enable IGF-1 to inhibit cell apoptosis and increase the production of cellular proteins.
What does IGF-1 receptor do?
This receptor mediates the effects of IGF-1, which is a polypeptide protein hormone similar in molecular structure to insulin. IGF-1 plays an important role in growth and continues to have anabolic effects in adults – meaning that it can induce hypertrophy of skeletal muscle and other target tissues.
What inhibits insulin-like growth factor?
AMG 479, a fully human anti-insulin-like growth factor receptor type I monoclonal antibody, inhibits the growth and survival of pancreatic carcinoma cells.
Which is the best inhibitor of the IGF-1R receptor?
Nordihydroguaiaretic acid (NDGA) is a cytotoxic insulin-like growth factor-I receptor (IGF-1R)/HER2 inhibitor and induces apoptosis. Nordihydroguaiaretic acid (NDGA) inhibits p300 and activates autophagy .
Is there homology between IGF-1R and insulin receptor?
There is a 60% homology between IGF-1R and the insulin receptor. The structures of the autophosphorylation complexes of tyrosine residues 1165 and 1166 have been identified within crystals of the IGF1R kinase domain. In response to ligand binding, the α chains induce the tyrosine autophosphorylation of the β chains.
How is IGF1R inhibitor used in diabetic nephropathy?
Objective: To explore the anti-inflammatory mechanism of IGF1R inhibitor in diabetic nephropathy. Methods: C57/BL6 mice were reared with high-fat diet for 8 weeks, then were injected 30 mg/kg streptozotocin intraperitoneally to induce type 2 diabetes.
What is the role of IGF-IR in prostate cancer?
Increased levels of the IGF-IR are expressed in the majority of primary and metastatic prostate cancer patient tumors. Evidence suggests that IGF-IR signaling is required for survival and growth when prostate cancer cells progress to androgen independence.