PKCeta is required for beta1gamma2/beta3gamma2- and PKD-mediated transport to the cell surface and the organization of the Golgi apparatus.
PKCeta is required for beta1gamma2/beta3gamma2- and PKD-mediated transport to the cell surface and the organization of the Golgi apparatus.
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DOI：
10.1083/jcb.200412089
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发表时间：
2005-04-11
期刊：
影响因子：
--
通讯作者：
Malhotra V
中科院分区：
文献类型：
--
作者：
Díaz Añel AM;Malhotra V
蛋白激酶D（PKD）与TGN中的二酰基甘油（DAG）池结合，并经历涉及异源三聚体GTP结合蛋白亚基βγ的活化过程以调节膜分裂。这种裂变反应用于在TGN处产生传输载流子，这些载流子在到达电池表面的途中。我们现在报道PKD被G蛋白亚基β1γ2和β3γ2通过高尔基体相关的PKCη特异性激活。损害PKCη的激酶活性-抑制蛋白从TGN转运至细胞表面。组成性激活的PKCη的表达引起高尔基体断裂，这被激酶失活形式的PKD抑制。我们的研究结果表明，βγ，PKCη和PKD串联作用，从TGN产生转运载体，它们的过度激活导致高尔基体的完全囊泡化。
Protein kinase D (PKD) binds to a pool of diacylglycerol (DAG) in the TGN and undergoes a process of activation that involves heterotrimeric GTP-binding protein subunits βγ to regulate membrane fission. This fission reaction is used to generate transport carriers at the TGN that are en route to the cell surface. We now report that PKD is activated specifically by G protein subunit β1γ2 and β3γ2 via the Golgi apparatus–associated PKCη. Compromising the kinase activity of PKCη-inhibited protein transport from TGN to the cell surface. Expression of constitutively activated PKCη caused Golgi fragmentation, which was inhibited by a kinase inactive form of PKD. Our findings reveal that βγ, PKCη, and PKD act in series to generate transport carriers from the TGN and their overactivation results in complete vesiculation of the Golgi apparatus.
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