|
| Status |
Public on Jun 10, 2016 |
| Title |
H3K36me3_48h_GW3965_Rep2 |
| Sample type |
SRA |
| |
|
| Source name |
H3K36me3_48h_GW3965
|
| Organism |
Homo sapiens |
| Characteristics |
cell line: HT29
cell type: colorectal adenocarcinoma
agent: GW3965
time: 48hr
chip antibody: anti-H3K36me3 (Abcam, ab9050)
|
| Treatment protocol |
HT29 were treated with DMSO, GW3965 (10uM), T0901317 (10uM) or rosiglitazone (10uM)
|
| Growth protocol |
HT29 cells were grown under recommended growth conditions
|
| Extracted molecule |
genomic DNA |
| Extraction protocol |
ChIP-seq was performed as previously described (Reddy et al. Molecular Cell 2013). RNA-seq was performed as previously outlned (Gertz et al. 2012)
Illumina Single End for ChIP-seq, Illumina Paired End for RNA-seq
|
| |
|
| Library strategy |
ChIP-Seq |
| Library source |
genomic |
| Library selection |
ChIP |
| Instrument model |
Illumina HiSeq 2000 |
| |
|
| Description |
Peaks with this histone modification were not called since it is found in gene bodies and does not make a canonical "binding" site.
|
| Data processing |
ChIP-seq and ChIP input control FASTQ files were aligned to hg19 female genome using Bowtie
Peak Calling was performed using MACS peak caller
Processed data files format and content: bed (Chromosome number, start position, stop position)
Genome_build: hg19 female
|
| |
|
| Submission date |
Jan 20, 2016 |
| Last update date |
May 15, 2019 |
| Contact name |
Daniel Savic |
| E-mail(s) |
daniel.savic@stjude.org
|
| Organization name |
St. Jude Children's Research Hospital
|
| Department |
Pharmaceutical Sciences
|
| Street address |
262 Danny Thomas Place
|
| City |
Memphis |
| State/province |
Tennessee |
| ZIP/Postal code |
38105 |
| Country |
USA |
| |
|
| Platform ID |
GPL11154 |
| Series (1) |
| GSE77039 |
Distinct gene regulatory programs define the inhibitory effects of LXRs and PPARG on cancer cell proliferation |
|
| Relations |
| BioSample |
SAMN04430566 |
| SRA |
SRX1538802 |
