14-3-3 proteins: an important regulator of autophagy in diseases

被引：0

作者：

Jia, Haoyuan ^{[1
,2
]}

Liang, Zhaofeng ^{[1
]}

Zhang, Xu ^{[1
]}

Wang, Juanjuan ^{[1
]}

Xu, Wenrong ^{[1
]}

Qian, Hui ^{[1
]}

机构：

[1] Jiangsu Univ, Sch Med, Key Lab Lab Med Jiangsu Prov, 301 Xuefu Rd, Zhenjiang 212013, Jiangsu, Peoples R China

[2] Nanjing Med Univ, Wuxi Peoples Hosp, Wuxi 214023, Jiangsu, Peoples R China

来源：

AMERICAN JOURNAL OF TRANSLATIONAL RESEARCH | 2017年 / 9卷 / 11期

基金：

中国国家自然科学基金;

关键词：

14-3-3; proteins; autophagy; cancer; neurodegenerative diseases; GASTRIC-CANCER CELLS; MOLECULAR-MECHANISMS; TUMORIGENESIS; GLIOBLASTOMA; INHIBITION; PHOSPHORYLATION; ANTAGONIZES; ACTIVATION; EXPRESSION; STARVATION;

D O I：

暂无

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Autophagy is a cell digestion process that determines cell fate by promoting cell survival or inducing cell death in a cell context-dependent manner. Several classical signaling pathways, such as phosphoinositide-3-kinase and mammalian target of rapamycin, tightly regulate autophagy. 14-3-3 proteins regulate various signaling pathways by phosphorylation-dependent binding with partner proteins. 14-3-3 proteins also regulate autophagy by binding with autophagy-related proteins such as Beclin-1 and hVPS34. This review summarizes the role of 14-3-3 proteins in the control of autophagy in cancer, neurodegenerative diseases and other pathological conditions.

引用

页码：4738 / 4746

页数：9

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