Genome-wide redistribution of BRD4 binding sites in transformation resistant cells

Han Si; Paola Scaffidi; Anand Merchant; Maggie Cam; Eric Stahlberg; Tom Misteli; Patricia Fernandez

doi:10.1016/j.gdata.2014.11.005

Genome-wide redistribution of BRD4 binding sites in transformation resistant cells

Genom Data. 2015 Mar 1:3:33-35. doi: 10.1016/j.gdata.2014.11.005.

Authors

Han Si¹, Paola Scaffidi², Anand Merchant¹, Maggie Cam³, Eric Stahlberg¹, Tom Misteli², Patricia Fernandez²

Affiliations

¹ CCRIFX, National Cancer Institute, NIH, Bethesda, Maryland, 20892.
² Cell Biology of Genomes Group, LRBGE, National Cancer Institute, NIH, Bethesda, Maryland, 20892.
³ OSTR, National Cancer Institute, NIH, Bethesda, Maryland, 20892.

Abstract

Hutchinson-Gilford progeria syndrome (HGPS) patients do not develop cancer despite a significant accumulation of DNA damage in their cells. We have recently reported that HGPS cells are refractory to experimental oncogenic transformation and we identified the bromodomain-containing 4 protein (BRD4) as a mediator of the transformation resistance. ChIP-sequencing experiments revealed distinct genome-wide binding patterns for BRD4 in HGPS cells when compared to control wild type cells. Here we provide a detailed description of the ChIP-seq dataset (NCBI GEO accession number GSE61325), the specific and common BRD4 binding sites between HGPS and control cells, and the data analysis procedure associated with the publication by Fernandez et al., 2014 in Cell Reports 9, 248-260 [1].

Abstract

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