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STK16 通过调节肌动蛋白动力学来控制高尔基体的组织和细胞周期。

STK16 regulates actin dynamics to control Golgi organization and cell cycle.

机构信息

High Magnetic Field Laboratory, Chinese Academy of Sciences, Hefei, Anhui, 230031, P. R. China.

University of Science and Technology of China, Hefei, Anhui, 230036, P. R. China.

出版信息

Sci Rep. 2017 Mar 15;7:44607. doi: 10.1038/srep44607.

DOI:10.1038/srep44607
PMID:28294156
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5353726/
Abstract

STK16 is a ubiquitously expressed, myristoylated, and palmitoylated serine/threonine protein kinase with underexplored functions. Recently, it was shown to be involved in cell division but the mechanism remains unclear. Here we found that human STK16 localizes to the Golgi complex throughout the cell cycle and plays important roles in Golgi structure regulation. STK16 knockdown or kinase inhibition disrupts actin polymers and causes fragmented Golgi in cells. In vitro assays show that STK16 directly binds to actin and regulates actin dynamics in a concentration- and kinase activity-dependent way. In addition, STK16 knockdown or kinase inhibition not only delays mitotic entry and prolongs mitosis, but also causes prometaphase and cytokinesis arrest. Therefore, we revealed STK16 as a novel actin binding protein that resides in the Golgi, which regulates actin dynamics to control Golgi structure and participate in cell cycle progression.

摘要

STK16 是一种普遍表达的、豆蔻酰化和棕榈酰化的丝氨酸/苏氨酸蛋白激酶,其功能尚未得到充分探索。最近的研究表明,它参与细胞分裂,但机制尚不清楚。在这里,我们发现人类 STK16 在整个细胞周期中定位于高尔基体复合物,并在高尔基体结构调节中发挥重要作用。STK16 敲低或激酶抑制破坏了肌动蛋白聚合物,并导致细胞中的高尔基体碎片化。体外实验表明,STK16 直接与肌动蛋白结合,并以浓度和激酶活性依赖的方式调节肌动蛋白动力学。此外,STK16 敲低或激酶抑制不仅延迟有丝分裂进入并延长有丝分裂,还导致前期和胞质分裂停滞。因此,我们揭示了 STK16 作为一种新的肌动蛋白结合蛋白,位于高尔基体中,它调节肌动蛋白动力学以控制高尔基体结构并参与细胞周期进程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ec/5353726/994ff8f7f45d/srep44607-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ec/5353726/a139770c1c43/srep44607-f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ec/5353726/04d4aa9574b6/srep44607-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ec/5353726/6aa9fa73ae66/srep44607-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ec/5353726/4eef44c847f1/srep44607-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ec/5353726/ea0231f4648d/srep44607-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ec/5353726/a5c50a312726/srep44607-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ec/5353726/994ff8f7f45d/srep44607-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ec/5353726/a139770c1c43/srep44607-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ec/5353726/62446691d151/srep44607-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ec/5353726/ef8922414ef2/srep44607-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ec/5353726/04d4aa9574b6/srep44607-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ec/5353726/6aa9fa73ae66/srep44607-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ec/5353726/4eef44c847f1/srep44607-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ec/5353726/ea0231f4648d/srep44607-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ec/5353726/a5c50a312726/srep44607-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ec/5353726/994ff8f7f45d/srep44607-f9.jpg

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