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蛋白激酶D调节源自反式高尔基体网络的细胞表面靶向运输载体的裂变。

Protein kinase D regulates the fission of cell surface destined transport carriers from the trans-Golgi network.

作者信息

Liljedahl M, Maeda Y, Colanzi A, Ayala I, Van Lint J, Malhotra V

机构信息

Biology Department, University of California, San Diego, La Jolla, CA 92093, USA.

出版信息

Cell. 2001 Feb 9;104(3):409-20. doi: 10.1016/s0092-8674(01)00228-8.

DOI:10.1016/s0092-8674(01)00228-8
PMID:11239398
Abstract

When a kinase inactive form of Protein Kinase D (PKD-K618N) was expressed in HeLa cells, it localized to the trans-Golgi network (TGN) and caused extensive tubulation. Cargo that was destined for the plasma membrane was found in PKD-K618N-containing tubes but the tubes did not detach from the TGN. As a result, the transfer of cargo from TGN to the plasma membrane was inhibited. We have also demonstrated the formation and subsequent detachment of cargo-containing tubes from the TGN in cells stably expressing low levels of PKD-K618N. Our results suggest that PKD regulates the fission from the TGN of transport carriers that are en route to the cell surface.

摘要

当蛋白激酶D的激酶失活形式(PKD-K618N)在HeLa细胞中表达时,它定位于反式高尔基体网络(TGN)并导致广泛的管状化。发现在含有PKD-K618N的管中有运往质膜的货物,但这些管并未从TGN脱离。结果,货物从TGN向质膜的转运受到抑制。我们还证明了在稳定表达低水平PKD-K618N的细胞中,含货物的管从TGN形成并随后脱离。我们的结果表明,PKD调节了正在运往细胞表面的运输载体从TGN的裂变。

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