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ERK1/2 在细胞衰老中的作用形成机制(综述)。

Mechanisms shaping the role of ERK1/2 in cellular senescence (Review).

机构信息

Research Institute of Digestive Diseases, Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.

Department of Pathology, Shenzhen Hospital of Southern Medical University, Shenzhen, Guangdong 518110, P.R. China.

出版信息

Mol Med Rep. 2019 Feb;19(2):759-770. doi: 10.3892/mmr.2018.9712. Epub 2018 Nov 29.

DOI:10.3892/mmr.2018.9712
PMID:30535440
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6323238/
Abstract

Senescence is a result of cellular stress and is a potential mechanism for regulating cancer. As a member of the mitogen‑activated protein kinase family, ERK1/2 (extracellular signal‑regulated protein kinase) has an important role in delivering extracellular signals to the nucleus, and these signals regulate the cell cycle, cell proliferation and cell development. Previous studies demonstrated that ERK1/2 is closely associated with cell aging; however other previous studies suggested that ERK1/2 exerts an opposite effect on aging models and target proteins, even within the same cell model. Recent studies demonstrated that the effect of ERK1/2 on aging is likely associated with its target proteins and regulators, negative feedback loops, phosphorylated ERK1/2 factors and ERK1/2 translocation from the cytoplasm to the nucleus. The present review aims to examine the mechanism of ERK1/2 and discuss its role in cellular outcomes and novel drug development.

摘要

衰老源自细胞应激,是调节癌症的一种潜在机制。ERK1/2(细胞外信号调节蛋白激酶)作为丝裂原活化蛋白激酶家族的一员,在将细胞外信号传递到细胞核的过程中发挥着重要作用,这些信号调节细胞周期、细胞增殖和细胞发育。先前的研究表明 ERK1/2 与细胞衰老密切相关;然而,其他先前的研究表明,ERK1/2 对衰老模型和靶蛋白的作用相反,即使在相同的细胞模型中也是如此。最近的研究表明,ERK1/2 对衰老的影响可能与其靶蛋白和调节剂、负反馈回路、磷酸化 ERK1/2 因子以及 ERK1/2 从细胞质向细胞核的转位有关。本综述旨在探讨 ERK1/2 的作用机制,并讨论其在细胞结果和新型药物开发中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c6d/6323238/358d523b63fb/MMR-19-02-0759-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c6d/6323238/b64ba9e64ab3/MMR-19-02-0759-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c6d/6323238/358d523b63fb/MMR-19-02-0759-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c6d/6323238/b64ba9e64ab3/MMR-19-02-0759-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c6d/6323238/358d523b63fb/MMR-19-02-0759-g01.jpg

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