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Journal of Lipid Research, Vol. 50, S132-S137, April 2009
Physiological consequences of disruption of mammalian phospholipid biosynthetic genes
* Group on Molecular and Cell Biology of Lipids and Department of Biochemistry, University of Alberta, Edmonton, Alberta T6G 2S2 Canada Research in the authors' labs was supported by grants from Canadian Institutes of Health Research and Heart and Stroke Foundation. D.E.V. holds the Canada Research Chair in Molecular and Cell Biology of Lipids and is a Scientist of the Alberta Heritage Foundation for Medical Research. Published, JLR Papers in Press, October 27, 2008.
1 To whom correspondence should be addressed. e-mail: dennis.vance{at}ualberta.ca (D.E.V.); jean.vance{at}ualberta.ca (J.V.)
By 1959, Eugene Kennedy and coworkers had outlined most pathways of phospholipid biosynthesis. In the next four decades, the emphasis was on enzymology and regulation of these pathways. In the last 12 years, several lines of mice with disrupted genes of phospholipid biosynthesis were generated. From this research, we have learned that embryonic lethality occurs in mice that lack choline kinase (CK)
Supplementary key words phosphatidylcholine phosphatidylethanolamine phosphatidylserine choline kinase CTP:phosphocholine cytidylyltransferase phosphatidylethanolamine N-methyltransferase phosphatidylserine synthase phosphatidylserine decarboxylase Abbreviations: apo, apolipoprotein; CD, choline-deficient; CK, choline kinase; CT, CTP:phosphocholine cytidylyltransferase; ER, endoplasmic reticulum; ET, CTP:phosphoethanolamine cytidylyltransferase; PC, phosphatidylcholine; PE, phosphatidylethanolamine; PEMT, phosphatidylethanolamine N-methyltransferase: PS, phosphatidylserine; PSD, PS decarboxylase; PSS, PS synthase; TG, triacylglycerol
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