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SRX2537518: GSM2476359: NRAS metastatic melanoma ChIP-BRD4 JQ1 (+) [SKmel147]; Homo sapiens; ChIP-Seq
1 ILLUMINA (NextSeq 500) run: 149.6M spots, 12G bases, 4.4Gb downloads

Submitted by: NCBI (GEO)
Study: Harnessing BET inhibitor sensitivity reveals AMIGO2 as a melanoma survival gene.
show Abstracthide Abstract
We utilize the transcriptional effects of BETi in melanoma and identify AMIGO2 as a direct target gene essential for melanoma cell survival both in vitro and in vivo. We further map the enhancer landscape of NHM and melanooma and show that genes regulated by super enhancers are expressed in higher levels, exihibit higher sensitivity to BETi, and over expressed in melanoma relative to NHM. In melanoma, AMIGO2 is regulated by super enhancers, which upon BETi lose their BRD2/BRD4 enrichment, resulting in AMIGO2 silencing. Overall design: We interogate two NHM culures and four melanoma cell lines for transcriptional changes upon BET inhibition and correlate those wiith changes in enhancer landscape and BRD2/4 occupancy at regulatory regions.
Sample: NRAS metastatic melanoma ChIP-BRD4 JQ1 (+) [SKmel147]
SAMN06294939 • SRS1957452 • All experiments • All runs
Organism: Homo sapiens
Library:
Instrument: NextSeq 500
Strategy: ChIP-Seq
Source: GENOMIC
Selection: ChIP
Layout: SINGLE
Construction protocol: For BRD2, BRD4 and MED1, 72x10^6 cells, were crosslinked with 1% PFA for 10 min at RT. ChIP was performed essentially as previously described (Roe, J.S., et al., BET Bromodomain Inhibition Suppresses the Function of Hematopoietic Transcription Factors in Acute Myeloid Leukemia. Mol Cell, 2015. 58(6): p. 1028-39). Libraries for ChIP-seq were done as previously described (Hasson D., et al., The octamer is the major form of CENP-A nucleosomes at human centromeres. Nat Struct Mol Biol. 2013 Jun;20(6):687-95).
Experiment attributes:
GEO Accession: GSM2476359
Links:
Runs: 1 run, 149.6M spots, 12G bases, 4.4Gb
Run# of Spots# of BasesSizePublished
SRR5228508149,645,48412G4.4Gb2017-11-22

ID:
3671619

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