Ubiquitin at the crossroad of cell death and survival

被引:14
作者
Chen, Yu-Shan
Qiu, Xiao-Bo [1 ]
机构
[1] Beijing Normal Univ, Coll Life Sci, Beijing 100875, Peoples R China
基金
中国国家自然科学基金;
关键词
Apoptosis; autophagy; BRUCE; caspase; NF-kappa B; p53; ubiquitin; ubiquitination; ACUTE MYELOID-LEUKEMIA; HIPPEL-LINDAU PROTEIN; CANCER-CELLS; LIGASE ACTIVITY; JNK1-MEDIATED PHOSPHORYLATION; NEDD8-ACTIVATING ENZYME; PROTEASOMAL DEGRADATION; APOPTOSIS PROTEIN; DEPENDENT PATHWAY; DOWN-REGULATION;
D O I
10.5732/cjc.012.10283
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Ubiquitination is crucial for cellular processes, such as protein degradation, apoptosis, autophagy, and cell cycle progression. Dysregulation of the ubiquitination network accounts for the development of numerous diseases, including cancer. Thus, targeting ubiquitination is a promising strategy in cancer therapy. Both apoptosis and autophagy are involved in tumorigenesis and response to cancer therapy. Although both are categorized as types of cell death, autophagy is generally considered to have protective functions, including protecting cells from apoptosis under certain cellular stress conditions. This review highlights recent advances in understanding the regulation of apoptosis and autophagy by ubiquitination.
引用
收藏
页码:640 / 647
页数:8
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