Expression profiles and ChIP on chip genomewide experiments with deltaCR2 mutant virus
ID:
状态:
发布时间Aug. 26, 2008
, 更新时间 May 3, 2014
, 提交时间 July 8, 2008,
物种:
Homo sapiens
摘要:
Adenovirus e1a induces quiescent human cells to divide. We found that e1a causes global relocalization of the RB-proteins (RB, p130, p107) and p300/CBP histone acetyltransferases on promoters that restricts H3K18ac to a limited set of genes to stimulate cell cycling and inhibit antiviral responses and cellular differentiation. Soon after expression, e1a binds transiently to cell cycle/growth genes, causing enrichment of p300/CBP, PCAF, H3K18ac, depletion of RB-proteins, and transcriptional activation. e1a also associates transiently with antiviral genes, causing enrichment for RB, p130, H4K16ac, increased nucleosome density, and repression. At later times, e1a and p107 bind mainly to development/differentiation genes, repressing transcription. The temporal order of e1a binding required its interactions with p300/CBP and RB-proteins. Our data uncover a defined transcriptional and epigenetic reprogramming leading to cellular transformation. Expression profiles and ChIP on chip genomewide experiments with deltaCR2 mutant virus
实验种类:
transcription profiling by array, ChIP-chip by tiling array