H3K4me3
生物
染色质
组蛋白
乙酰化
细胞生物学
抄写(语言学)
组蛋白H3
染色质免疫沉淀
转录因子
P300-CBP转录因子
DNA损伤
表观遗传学
遗传学
DNA
基因
发起人
基因表达
组蛋白乙酰转移酶
哲学
语言学
作者
Zhanyun Tang,Wei Yi Chen,Miho Shimada,Uyen Nguyen,Jaehoon Kim,Xiao Jian Sun,Toru Sengoku,Robert K. McGinty,Joseph Fernandez,Tom W. Muir,Robert G. Roeder
出处
期刊:Cell
[Elsevier]
日期:2013-07-01
卷期号:154 (2): 297-310
被引量:149
标识
DOI:10.1016/j.cell.2013.06.027
摘要
The H3K4me3 mark in chromatin is closely correlated with actively transcribed genes, although the mechanisms involved in its generation and function are not fully understood. In vitro studies with recombinant chromatin and purified human factors demonstrate a robust SET1 complex (SET1C)-mediated H3K4 trimethylation that is dependent upon p53- and p300-mediated H3 acetylation, a corresponding SET1C-mediated enhancement of p53- and p300-dependent transcription that reflects a primary effect of SET1C through H3K4 trimethylation, and direct SET1C-p53 and SET1C-p300 interactions indicative of a targeted recruitment mechanism. Complementary cell-based assays demonstrate a DNA-damage-induced p53-SET1C interaction, a corresponding enrichment of SET1C and H3K4me3 on a p53 target gene (p21/WAF1), and a corresponding codependency of H3K4 trimethylation and transcription upon p300 and SET1C. These results establish a mechanism in which SET1C and p300 act cooperatively, through direct interactions and coupled histone modifications, to facilitate the function of p53.
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