期刊
NATURE GENETICS
卷 27, 期 1, 页码 121-124出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/83685
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资金
- NHLBI NIH HHS [HL24841] Funding Source: Medline
Mice carrying mutations in the fatty liver dystrophy (fld) gene have features of human lipodystrophy(1), a genetically heterogeneous group of disorders characterized by loss of body fat, fatty liver hypertriglyceridemia and insulin resistance(2-4). Through positional cloning, we have isolated the gene responsible and characterized two independent mutant alleles, fld and fld(2J). The gene (Lpin1) encodes a novel nuclear protein which we have named lipin. Consistent with the observed reduction of adipose tissue mass in fld and fld(2J) mice, wild-type Lpin1 mRNA is expressed at high levels in adipose tissue and is induced during differentiation of 3T3-L1 pre-adipocytes. Our results indicate that lipin is required for normal adipose tissue development, and provide a candidate gene for human lipodystrophy. Lipin defines a novel family of nuclear proteins containing at least three members in mammalian species, and homologs in distantly related organisms from human to yeast.
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