Suppr超能文献

二酰甘油激酶η在应对渗透压休克时与凋亡信号调节激酶3共定位并相互作用。

Diacylglycerol kinase η colocalizes and interacts with apoptosis signal-regulating kinase 3 in response to osmotic shock.

作者信息

Suzuki Yuji, Asami Maho, Takahashi Daisuke, Sakane Fumio

机构信息

Department of Chemistry, Graduate School of Science, Chiba University, Chiba 263-8522, Japan.

Department of Pharmaceutical Health Care and Sciences, Kyushu University, Fukuoka 812-8582, Japan.

出版信息

Biochem Biophys Rep. 2021 Apr 27;26:101006. doi: 10.1016/j.bbrep.2021.101006. eCollection 2021 Jul.

Abstract

Diacylglycerol kinase (DGK) η translocates from the cytoplasm to punctate vehicles via osmotic shock. Apoptosis signal-regulating kinase (ASK) 3 (MAP kinase kinase kinase (MAPKKK) 15) is also reported to respond to osmotic shock. Therefore, in the present study, we examined the subcellular localization of DGKη and ASK3 expressed in COS-7 cells under osmotic stress. We found that DGKη was almost completely colocalized with ASK3 in punctate structures in response to osmotic shock. In contrast, DGKδ, which is closely related to DGKη structurally, was not colocalized with ASK3, and DGKη failed to colocalize with another MAPKKK, C-Raf, even under osmotic stress. The structures in which DGKη and ASK3 localized were not stained with stress granule makers. Notably, DGKη strongly interacted with ASK3 in an osmotic shock-dependent manner. These results indicate that DGKη and ASK3 undergo osmotic shock-dependent colocalization and associate with each other in specialized structures.

摘要

二酰甘油激酶(DGK)η通过渗透压休克从细胞质转位至点状小泡。据报道,凋亡信号调节激酶(ASK)3(丝裂原活化蛋白激酶激酶激酶(MAPKKK)15)也对渗透压休克有反应。因此,在本研究中,我们检测了在渗透压应激下COS-7细胞中表达的DGKη和ASK3的亚细胞定位。我们发现,在渗透压休克反应中,DGKη几乎完全与ASK3在点状结构中共定位。相比之下,在结构上与DGKη密切相关的DGKδ未与ASK3共定位,即使在渗透压应激下,DGKη也未能与另一种MAPKKK即C-Raf共定位。DGKη和ASK3定位的结构未被应激颗粒标志物染色。值得注意的是,DGKη以渗透压休克依赖的方式与ASK3强烈相互作用。这些结果表明,DGKη和ASK3发生渗透压休克依赖的共定位,并在特殊结构中相互关联。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b961/8100535/4ce2e1b51ed0/gr1.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验