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논문 기본 정보

자료유형
학술저널
저자정보
Lee, Seong-Won (School of Biological Sciences, Seoul National University) Seong, Min-Woo (School of Biological Sciences, Seoul National University) Jeon, Young-Joo (School of Biological Sciences, Seoul National University) Chung, Chin-Ha (School of Biological Sciences, Seoul National University)
저널정보
한국통합생물학회 Animal cells and systems Animal cells and systems 제16권 제3호
발행연도
2012.1
수록면
173 - 182 (10page)

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The p53 protein plays a pivotal role in tumor suppression. The cellular level of p53 is normally kept low by proteasome-mediated degradation, allowing cell cycle progression and cell proliferation. Under stress conditions, such as DNA damage, p53 is stabilized and activated through various post-translational modifications of itself as well as of its regulatory proteins for induction of the downstream genes responsible for cell cycle arrest, DNA repair, and apoptosis. Therefore, the level of p53 should be tightly regulated for normal cell growth and for prevention of the accumulation of mutations in DNA under stress conditions, which otherwise would lead to tumorigenesis. Since the discovery of Mdm2, a critical ubiquitin E3 ligase that destabilizes p53 in mammalian cells, nearly 20 different E3 ligases have been identified and shown to function in the control of stability, nuclear export, translocation to chromatin or nuclear foci, and oligomerization of p53. So far, a large number of excellent reviews have been published on the control of p53 function in various aspects. Therefore, this review will focus only on mammalian ubiquitin E3 ligases that mediate proteasome-dependent degradation of p53.

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