Structure and apoptotic function of p73

被引:46
|
作者
Yoon, Mi-Kyung [1 ]
Ha, Ji-Hyang [1 ]
Lee, Min-Sung [1 ,2 ]
Chi, Seung-Wook [1 ,2 ]
机构
[1] KRIBB, Funct Genom Res Ctr, Struct Biol & Nanopore Res Lab, Taejon 305806, South Korea
[2] Univ Sci & Technol, Dept Bioanalyt Sci, Taejon 305350, South Korea
关键词
Apoptosis; Cancer therapy; p53 protein family; p73; Structure; RECEPTOR SAM DOMAIN; PROTEIN STABILITY; BCL-2; FAMILY; MEMBRANE PERMEABILIZATION; TRANSACTIVATION DOMAIN; P53-RELATED PROTEIN; LIGASE ITCH; P53; HOMOLOG; DNA-BINDING; MITOCHONDRIA;
D O I
10.5483/BMBRep.2015.48.2.255
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
p73 is a structural and functional homologue of the p53 tumor suppressor protein. Like p53, p73 induces apoptosis and cell cycle arrest and transactivates p53-responsive genes, conferring its tumor suppressive activity. In addition, p73 has unique roles in neuronal development and differentiation. The importance of p73-induced apoptosis lies in its capability to substitute the pro-apoptotic activity of p53 in various human cancer cells in which p53 is mutated or inactive. Despite the great importance of p73-induced apoptosis in cancer therapy, little is known about the molecular basis of p73-induced apoptosis. In this review, we discuss the p73 structures reported to date, detailed structural comparisons between p73 and p53, and current understanding of the transcription-dependent and -independent mechanisms of p73-induced apoptosis.
引用
收藏
页码:81 / 90
页数:10
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