16aa peptide of Mouse Lipin-3. The actions of insulin culminate in changes in the phosphorylation state of a number of downstream targets including phosphatidylinositol 3-OH kinase (PI3-kinase). Activation of PI3-kinase is central to insulin-stimulated phosphorylation in fat cells. In adipocytes, PI3 is involved in activation of protein kinase B (PKB), glycogen synthase, transitional regulators, 4E-BP1, p70s6k and mTOR protein (mammalian target of rapamycin). The kinase activity of mTOR functions in nutrient sensing pathway that maintains a proper balance of aa availability, protein synthesis and cell growth. Most importantly, mTOR controls the phosphorylation of a newly discovered protein Lipin-1, required for normal adipose tissue development and metabolism. The mutation in Lpin-1 gene results in immature adipocytes and thus in fatty liver dystrophy (fld) phenotype in mice and in lipodystrophy, a group of rare human diseases. These phenotypes are characterized by a triglyceride-filled fatty liver, loss of body fat, hypertrigyceridemia, insulin resistance, increased susceptibility to atherosclerosis, reduced fertility, reduced plasma Leptin and a progressive neuropathy affecting peripheral nerves in adulthood. Lipin defines a family of nuclear proteins containing at least three members in human and mouse: Lipin-1, Lipin-2 and Lipin-3. All Lipin members contain a nuclear signal seq, a highly conserved amino- (NLIP) and a carboxy-terminal (CLIP) domains. Lipin-3: The human (LPIN3) and mouse Lipin3 genes have been mapped at chromosomes 20q and 2, respectively. The overall aa seq of mouse Lipin-3 (848aa) is 46% and 48% identical to mouse Lipin-1 (891aa, 140kD) and Lipin-2 ((891aa), respectively.
Reinheit:
Highly purified
Formulierung:
Supplied as a liquid in PBS, pH 7.2
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