Kuge Osamu, Nishijima Masahiro
Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku, Tokyo 162-8640.
J Biochem. 2003 Apr;133(4):397-403. doi: 10.1093/jb/mvg052.
In mammalian cells, phosphatidylserine (PtdSer) is synthesized through the action of the endoplasmic reticulum enzymes, PtdSer synthase 1 and 2, and the decarboxylation of PtdSer accounts for the majority of phosphatidylethanolamine (PtdEtn) synthesis. PtdSer decarboxylation for PtdEtn formation occurs in the mitochondria. In addition, the transport of PtdSer from the endoplasmic reticulum to the mitochondria is probably a rate limiting step for PtdEtn synthesis through the decarboxylation pathway. Therefore, the regulation of PtdSer synthesis and its intracellular transport appear to be essential events for the maintenance of normal cellular PtdSer and PtdEtn levels. Here we describe the current understanding of the regulation of PtdSer biosynthesis and the transport of PtdSer from the ER to the mitochondria in mammalian cells.
在哺乳动物细胞中，磷脂酰丝氨酸（PtdSer）通过内质网酶磷脂酰丝氨酸合成酶1和2的作用合成，而磷脂酰丝氨酸的脱羧作用占磷脂酰乙醇胺（PtdEtn）合成的大部分。用于形成PtdEtn的PtdSer脱羧作用发生在线粒体中。此外，PtdSer从内质网到线粒体的转运可能是通过脱羧途径合成PtdEtn的限速步骤。因此，PtdSer合成及其细胞内转运的调节似乎是维持正常细胞PtdSer和PtdEtn水平的关键事件。在此，我们描述了目前对哺乳动物细胞中PtdSer生物合成调节以及PtdSer从内质网到线粒体转运的理解。
