文章基本信息

标题：Physiological consequences of disruption of mammalian phospholipid biosynthetic genes
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作者：Dennis E. Vance ; Jean E. Vance
期刊名称：JLR Papers In Press
印刷版ISSN：0022-2275
电子版ISSN：1539-7262
出版年度：2009
卷号：50
期号：Supplement
页码：S132-S137
DOI：10.1194/jlr.R800048-JLR200
语种：English
出版社：American Society for Biochemistry and Molecular Biology
摘要：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) α, CTP:phosphocholine cytidylyltransferase α, CTP:phosphoethanolamine cytidylyltransferase, or phosphatidylserine decarboxylase. Whereas mice that lack CK β are viable but develop hindlimb muscular dystrophy and neonatal bone deformity. Mice that lack CTP:phosphocholine cytidylytransferase β have gonadal dysfunction and defective axon branching. Mice that lack phosphatidylethanolamine N -methyltransferase exhibit no phenotype until fed a choline-deficient diet, which leads to rapid liver failure. Future research should extend our knowledge about the function of these and other enzymes of phospholipid biosynthesis.