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二聚体多囊蛋白在反式高尔基体网络中调节膜裂变以形成运输载体。

Dimeric PKD regulates membrane fission to form transport carriers at the TGN.

作者信息

Bossard Carine, Bresson Damien, Polishchuk Roman S, Malhotra Vivek

机构信息

Section of Cell and Developmental Biology, University of California, San Diego, La Jolla, CA 92093, USA.

出版信息

J Cell Biol. 2007 Dec 17;179(6):1123-31. doi: 10.1083/jcb.200703166.

Abstract

Protein kinase D (PKD) is recruited to the trans-Golgi network (TGN) through interaction with diacylglycerol (DAG) and is required for the biogenesis of TGN to cell surface transport carriers. We now provide definitive evidence that PKD has a function in membrane fission. PKD depletion by siRNA inhibits trafficking from the TGN, whereas expression of a constitutively active PKD converts TGN into small vesicles. These findings demonstrate that PKD regulates membrane fission and this activity is used to control the size of transport carriers, and to prevent uncontrolled vesiculation of TGN during protein transport.

摘要

蛋白激酶D(PKD)通过与二酰基甘油(DAG)相互作用被招募到反式高尔基体网络(TGN),并且是TGN到细胞表面运输载体生物发生所必需的。我们现在提供了确凿的证据,证明PKD在膜裂变中发挥作用。通过小干扰RNA(siRNA)使PKD缺失会抑制从TGN的运输,而组成型活性PKD的表达则会将TGN转化为小囊泡。这些发现表明,PKD调节膜裂变,并且这种活性被用于控制运输载体的大小,并防止在蛋白质运输过程中TGN发生不受控制的囊泡化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1872/2140039/7caa347a719c/jcb1791123f01.jpg

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