Singhal 2016, ChIP-seq and reChIP for ESR1 and PGR in hormone treated parental (PR+) and PR- T47D cells.
Description
ChIP-seq against ESR1 and PRG was carried out in ER+PR+ parental T47D cells
and PR-deficient T47D cells under different conditions: vehicle, E2 45 min,
R5020 45 min and E2R5020 45 min. In addition, ChIP followed by ChIP
(reChIP-seq) was carried out in order to map hormone receptor binding sites
simultaneously occupied by ESR1 and PRG. Separate input controls are provided
for ChIP-seq and reChIP-seq experiments.
Source
- Raw data was downloaded from SRA, bioprojects:
PRJNA318944
- Input file format: FASTQ
- Download date: 14-2-2022
Samples
From H. sapiens (Feb 2009 GRCh37/hg19).
Notes on samples nomenclature:
ReChIP-seq samples have target name "ESR1+PRG" in the second field of the target
description.
Input controls for reChIP-seq experiments are identified by the tag "reChIP" in
the fourth field of the description, which is usually occupied by a replicate
identifier. For ChIP-seq samples, this field is left blank.
Technical Notes
FASTQ files were extracted from SRA files using fastq-dump
(
SRA
toolkit v2.5.0) and mapped to the genome
using
Bowtie v1.2.2.
SAM files were then converted to BAM
using
samtools v1.9
and to BED using bamToBed v2.27.0
(
bedtools).
BED to SGA conversion was carried out using bed2sga
(
ChIP-Seq v. 1.5.5).
For reproducibility purposes, the scripts used for generating the SGA files are posted here:
singhal16_scripts.tar.gz
References
-
Singhal H, Greene ME, Tarulli G, Zarnke AL, Bourgo RJ, Laine M, Chang YF, Ma S,
Dembo AG, Raj GV, Hickey TE, Tilley WD, Greene GL.
Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors in breast cancer
Sci Adv. 2016 Jun 24;2(6):e1501924. doi: 10.1126/sciadv.1501924.
27386569
-
GEO series
GSE80367:
Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors in breast cancer. [ChIP-seq]
Last update: 08 Jul 2022
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