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pmid:25478319

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

Genomics data · 2015 doi:10.1016/j.gdata.2014.11.005

Paper

complete

Experiment

complete

Data

partial

Analysis

partial

Execution

absent

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title
Genome-wide redistribution of BRD4 binding sites in transformation resistant cells.
doi
10.1016/j.gdata.2014.11.005
pmid
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Han Si
[1]
Paola Scaffidi
[2]
Anand Merchant
[3]
Maggie Cam
[4]
Eric Stahlberg
[5]
Tom Misteli
[6]
Patricia Fernandez
journal
Genomics data
year
2015
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].
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ChIP-sequencing experiments revealed distinct genome-wide binding patterns for BRD4 in HGPS cells when compared to control wild type cells.
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Given the reported binding nature of BRD4 [9], 200 bp window size and 400 bp gap size were chosen in the peak calling step using SICER.
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BRD4 binding sites in transformed fibroblasts
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