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蛋白激酶 D 在氧化应激中的功能和调节:同工型的故事。

Function and Regulation of Protein Kinase D in Oxidative Stress: A Tale of Isoforms.

机构信息

Department of Cellular and Molecular Medicine, Faculty of Medicine, KU Leuven, Leuven, Belgium.

Leuven Cancer Institute (LKI), KU Leuven, Leuven, Belgium.

出版信息

Oxid Med Cell Longev. 2018 Apr 26;2018:2138502. doi: 10.1155/2018/2138502. eCollection 2018.

DOI:10.1155/2018/2138502
PMID:29854077
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5944262/
Abstract

Oxidative stress is a condition that arises when cells are faced with levels of reactive oxygen species (ROS) that destabilize the homeostatic redox balance. High levels of ROS can cause damage to macromolecules including DNA, lipids, and proteins, eventually resulting in cell death. Moderate levels of ROS however serve as signaling molecules that can drive and potentiate several cellular phenotypes. Increased levels of ROS are associated with a number of diseases including neurological disorders and cancer. In cancer, increased ROS levels can contribute to cancer cell survival and proliferation via the activation of several signaling pathways. One of the downstream effectors of increased ROS is the protein kinase D (PKD) family of kinases. In this review, we will discuss the regulation and function of this family of ROS-activated kinases and describe their unique isoform-specific features, in terms of both kinase regulation and signaling output.

摘要

氧化应激是一种细胞在面对不稳定的内稳态氧化还原平衡的活性氧(ROS)水平时出现的情况。高水平的 ROS 会对包括 DNA、脂质和蛋白质在内的大分子造成损害,最终导致细胞死亡。然而,中等水平的 ROS 可以作为信号分子,驱动和增强几种细胞表型。ROS 水平的升高与多种疾病有关,包括神经紊乱和癌症。在癌症中,ROS 水平的升高可以通过激活几种信号通路促进癌细胞的存活和增殖。ROS 水平升高的下游效应物之一是蛋白激酶 D(PKD)家族激酶。在这篇综述中,我们将讨论这个 ROS 激活激酶家族的调节和功能,并描述它们在激酶调节和信号输出方面独特的同工型特异性特征。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46c4/5944262/5f463e5edb0d/OMCL2018-2138502.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46c4/5944262/ade46522a9b6/OMCL2018-2138502.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46c4/5944262/1a9c5c0a28b4/OMCL2018-2138502.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46c4/5944262/5f463e5edb0d/OMCL2018-2138502.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46c4/5944262/ade46522a9b6/OMCL2018-2138502.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46c4/5944262/1a9c5c0a28b4/OMCL2018-2138502.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46c4/5944262/5f463e5edb0d/OMCL2018-2138502.003.jpg

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