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Publication : Lipopenia and skin barrier abnormalities in DGAT2-deficient mice.

First Author  Stone SJ Year  2004
Journal  J Biol Chem Volume  279
Issue  12 Pages  11767-76
PubMed ID  14668353 Mgi Jnum  J:88742
Mgi Id  MGI:3036977 Doi  10.1074/jbc.M311000200
Citation  Stone SJ, et al. (2004) Lipopenia and skin barrier abnormalities in DGAT2-deficient mice. J Biol Chem 279(12):11767-76
abstractText  The synthesis of triglycerides is catalyzed by two known acyl-CoA:diacylglycerol acyltransferase (DGAT) enzymes. Although they catalyze the same biochemical reaction, these enzymes share no sequence homology, and their relative functions are poorly understood. Gene knockout studies in mice have revealed that DGAT1 contributes to triglyceride synthesis in tissues and plays an important role in regulating energy metabolism but is not essential for life. Here we show that DGAT2 plays a fundamental role in mammalian triglyceride synthesis and is required for survival. DGAT2-deficient (Dgat2(-/-)) mice are lipopenic and die soon after birth, apparently from profound reductions in substrates for energy metabolism and from impaired permeability barrier function in the skin. DGAT1 was unable to compensate for the absence of DGAT2, supporting the hypothesis that the two enzymes play fundamentally different roles in mammalian triglyceride metabolism.
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