85-1401-99　Lipin 1, Mouse, Control Peptide 100ug　L2497-01B

特徴

• 16aa peptide (111-126aa) of Mouse Lipin-1 (1).
• 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). 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. Besides Lipin-1, there are at least 2 more nuclear proteins (Lipin-2 and Lipin-3) in human and mouse lipin families. All lipin members contain a nuclear signal seq, a highly conserved amino- (NLIP) and a carboxy-terminal (CLIP) domains.
• Lipin-1: The human and mouse LPIN-1 genes have been mapped at chromosomes 2p21 and 12, respectively. A region (POMC) on this same chromosome also encodes pro-opiomelanocortin, a locus linked to total adiposity and the levels of plasma protein Leptin. The mouse Lipin-1 is a 140kD (891 aa) protein with many potential phosphorylated sites. The overall aa seq of mouse Lipin-1 is over 46 and 49% identical to mouse Lipin-2 and Lipin-3, respectively. The seqs of human and mouse Lipin-1 are over 88% identical. Lpin-1 mRNA is prominently expressed in adipose tissue, skeletal muscle and testis with lower expression in kidney, lung, brain and liver. A Gly84Arg mutation in Lipin-1 alters the protein's subcellular localization from nuclear to cytoplasmic and impairs its activity. The mutation in Lpin-1 gene leads to Lipin-1 deficiency which results in the development of immature adipocytes in fatty liver dystrophy (fld) phenotype in mice and in a group of rare human diseases called lipodystrophy. These phenotypes are characterized by a triglyceride-filled fatty liver, loss of body fat, hypertrigyceridemia, glucose intolerance, insulin resistance, increased susceptibility to atherosclerosis, reduced fertility, reduced plasma Leptin and a progressive neuropathy affecting peripheral nerves in adulthood.