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SRX835578: GSM1581343: Mock_ChIP; Homo sapiens; ChIP-Seq
1 ILLUMINA (Illumina HiSeq 2000) run: 246.5M spots, 12.3G bases, 8.1Gb downloads

Submitted by: Gene Expression Omnibus (GEO)
Study: UTX inhibition as selective epigenetic therapy against TAL1-driven T cell acute lymphoblastic leukemia
show Abstracthide Abstract
We performed ChIP-Seq in Jurkat T-ALL cells to identify UTX binding sites across the genome. We then compared UTX binding sites (this study) with TAL1 binding sites (Data from Palii, 2011 GSE25000), and found a high degree of overlap between TAL1 and UTX in Jurkat T-All cells. Indeed, over 80% of TAL1 binding sites overlap with UTX. Overall design: Using ChIP-Seq, we identified UTX binding across the genome in Jurkat T-ALL cells. We then compared the binding sites of UTX and TAL1 (Data from Palii, 2011 GSE25000).
Sample: Mock_ChIP
SAMN03280486 • SRS813476 • All experiments • All runs
Organism: Homo sapiens
Library:
Instrument: Illumina HiSeq 2000
Strategy: ChIP-Seq
Source: GENOMIC
Selection: ChIP
Layout: SINGLE
Construction protocol: Binding of UTX transcription factor was measured using a ChIP protocol as previously described (Palii, 2011). Chromatin from 1x10^8 cells was fragmented to a size range of 100-300 bases with a Bioruptor (Diagenode) at 4 degrees C. Solubilized chromatin was immunoprecipitated with an antibody against UTX (home made 9838P mixed with A302-374A) or an isotype IgG control. Antibody-chromatin complexes were pulled-down using Dynabeads-Protein A, washed and eluted. After cross-link reversal and proteinase K treatment, immunoprecipitated DNA was extracted with phenol-chloroform. ChIPed DNA was amplified using the Illumina protocol with modifications described in (Palii, 2011).
Experiment attributes:
GEO Accession: GSM1581343
Links:
External link:
Runs: 1 run, 246.5M spots, 12.3G bases, 8.1Gb
Run# of Spots# of BasesSizePublished
SRR1748013246,516,16012.3G8.1Gb2016-02-01

ID:
1185353

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