Trichostatin A activates p18INK4c gene:: differential activation and cooperation with p19INK4d gene

被引：12

作者：

Yokota, T ^{[1
]}

Matsuzaki, Y ^{[1
]}

Sakai, T ^{[1
]}

机构：

[1] Kyoto Prefectural Univ Med, Grad Sch Med Sci, Dept Mol Targeting Canc Prevent, Kamigyo Ku, Kyoto 6028566, Japan

来源：

FEBS LETTERS | 2004年 / 574卷 / 1-3期

关键词：

historic deacetylase inhibitor; TSA; p18(INK4c); p19(INK4d); promoter activation;

D O I：

10.1016/j.febslet.2004.08.025

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：

We have reported that histone deacetylase (HDAC) inhibitors activate a member of the INK4 family, the p19(INK4d) gene, causing G1 phase arrest. We report here that HDAC inhibitor, Trichostatin A, activates another member of the INK4 family, the p18(INK4c) gene, through its promoter in Jurkat cells. Interestingly, the activation patterns of the p18(INK4c) gene were different from those of p19(INK4d). Furthermore, mouse embryo fibroblasts lacking p18(Ink4c) or p18(Ink4c)/p19(Ink4d) were resistant to the growth inhibitory effects of TSA as compared to their wildtype counterpart. Our findings suggest that p18(INK4c) is involved in TSA-mediated cell growth inhibition and cooperates with p19(INK4d). (C) 2004 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：171 / 175

页数：5

共 34 条

[1] Haploinsufficiency of p18INK4c sensitizes mice to carcinogen-induced tumorigenesis [J].