PKD 调节膜裂变以产生从 TGN 到质膜表面的运输载体。
PKD regulates membrane fission to generate TGN to cell surface transport carriers.
机构信息
Center for Genomic Regulation, Dr. Aiguader 88, Barcelona, Spain.
出版信息
Cold Spring Harb Perspect Biol. 2011 Feb 1;3(2):a005280. doi: 10.1101/cshperspect.a005280.
The serine/threonine protein kinase D (PKD) is recruited to the trans-Golgi network (TGN) by binding diacylglycerol (DAG) and the ARF1 GTPase. PKD, at the TGN, promotes the production of phosphatidylinositol-4 phosphate (PI4P) by activating the lipid kinase phophatidylinositol 4-kinase IIIß (PI4KIIIß). PI4P recruits proteins such as oxysterol-binding protein 1 (OSBP) and ceramide transport protein (CERT) that control sphingolipid and sterol levels at the TGN. CERT mediated transport of ceramide to the TGN, we suggest, is used for increasing the local production and concentration of DAG. Once the crucial concentration of DAG is achieved, OSBP and CERT dissociate from the TGN on phosphorylation by PKD and DAG is sequentially converted into phosphatidic acid (PA) and lyso-PA (LPA). Therefore, the net effect of the activated PKD at the TGN is the sequential production of the modified lipids DAG, PA, and LPA that are necessary for membrane fission to generate cell surface specific transport carriers.
丝氨酸/苏氨酸蛋白激酶 D（PKD）通过与二酰基甘油（DAG）和 ARF1 GTPase 结合而被招募到反式高尔基体网络（TGN）。PKD 在 TGN 处通过激活脂质激酶磷脂酰肌醇 4-激酶 IIIβ（PI4KIIIβ）促进磷脂酰肌醇-4-磷酸（PI4P）的产生。PI4P 招募诸如甾醇结合蛋白 1（OSBP）和神经酰胺转运蛋白（CERT）等蛋白，这些蛋白控制 TGN 处的鞘脂和固醇水平。我们认为，CERT 介导的神经酰胺向 TGN 的运输用于增加 DAG 的局部产生和浓度。一旦达到关键的 DAG 浓度，OSBP 和 CERT 通过 PKD 的磷酸化从 TGN 上解离，并且 DAG 依次转化为磷脂酸（PA）和溶血磷脂酸（LPA）。因此，激活的 PKD 在 TGN 上的净效应是顺序产生必需的修饰脂质 DAG、PA 和 LPA，这些脂质对于产生细胞膜特异性运输载体的膜裂变是必需的。
Zotero 插件