송재환 교수연구실에서는 최근 tumor suppressor인 p21의 acetylation의 조절기작에 대한 논문을 Cell Death and Differentiation의 advance online publication으로 게재 하였으며

이민식 박사과정 학생이 제일저자로 참여하였습니다. 관심 있으신 분들은 http://www.nature.com/cdd/journal/vaop/ncurrent/index.html 에서 이 논문을 download 받으실 수 있습니다.

Title: Stabilization of p21 (Cip1/WAF1) following Tip60-dependent acetylation is required for p21-mediated DNA damage response

(http://www.nature.com/cdd/journal/vaop/ncurrent/index.html)

Abstract

The molecular mechanisms controlling post-translational modifications of p21 have been pursued assiduously in recent years. Here, utilizing mass-spectrometry analysis and site-specific acetyl-p21 antibody, two lysine residues of p21, located at aminoacid sites 161 and 163, were identified as Tip60-mediated acetylation targets for the first time. Detection of adriamycin-induced p21 acetylation, which disappeared after Tip60 depletion with concomitant destabilization of p21 and disruption of G1 arrest, suggested that Tip60-mediated p21 acetylation is necessary for DNA damage-induced cell-cycle regulation. The ability of 2KQ, a mimetic of acetylated p21, to induce cell-cycle arrest and senescence was significantly enhanced in p21 null MEFs compared with those of cells expressing wild-type p21. Together, these observations demonstrate that Tip60-mediated p21 acetylation is a novel and essential regulatory process required for p21-dependent DNA damage-induced cell-cycle arrest. Cell Death and Differentiation advance online publication, 14 December 2012; doi:10.1038/cdd.2012.159

First author of CDD paper

Lee, Min-Sik