Transcriptomics

Dataset Information

2

P53 and p73 ChIP-chip experiments in HCT116-3(6) cells


ABSTRACT: The p53-family of transcription factors share a highly homologous DNA binding domain and have overlapping and distinct biological functions. Using chromatin immunoprecipitation in combination with NimbleGen promoter arrays and a Model-based Algorithm for Promoter arrays (MAP), we performed a direct comparison of the promoter occupancy profiles of p53 and p73 before and after treatment with hydroxyurea (HU). We have found that p53 and p73 bind to common promoters before HU treatment. After HU treatment, we found that p53-bound promoters are likely to also bind p73, but p73 binds to additional promoters that that do not bind p53. Among them, we showed that p73 but not p53 is recruited to the promoter of MLH3, which encodes a mismatch repair protein. The differential effects of HU on the promoter occupancy profiles of p53 and p73 suggest that these related transcription factors have divergent functions in DNA damage response. The main goal of this study is to examine the effect of HU on the promoter occupancy profiles of p53 and p73. One biological sample from HCT116-(6) cells treated with or without Hydroxyurea was subjected to ChIP-chip analysis using a model based algorithm for promoter arrays (MAP).

ORGANISM(S): Homo sapiens  

SUBMITTER: Jean Y Wang   Xin Lu  Yong Jiang  Vera Huang 

PROVIDER: E-GEOD-12224 | ArrayExpress | 2009-06-30

SECONDARY ACCESSION(S): GSE12224PRJNA113679

REPOSITORIES: GEO, ArrayExpress

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Publications

Effect of hydroxyurea on the promoter occupancy profiles of tumor suppressor p53 and p73.

Huang Vera V   Lu Xin X   Jiang Yong Y   Wang Jean Y J JY  

BMC biology 20090626


The p53 tumor suppressor and its related protein, p73, share a homologous DNA binding domain, and mouse genetics studies have suggested that they have overlapping as well as distinct biological functions. Both p53 and p73 are activated by genotoxic stress to regulate an array of cellular responses. Previous studies have suggested that p53 and p73 independently activate the cellular apoptotic program in response to cytotoxic drugs. The goal of this study was to compare the promoter-binding activi  ...[more]

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