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Series GSE45738 Query DataSets for GSE45738
Status Public on Aug 18, 2013
Title Addiction of t(8;21) and inv(16) AML to native RUNX1 [ChIP-Seq data]
Organism Homo sapiens
Experiment type Genome binding/occupancy profiling by high throughput sequencing
Summary Cancer cells maintain a sensitive balance between growth-promoting oncogenes and apoptosis inhibitors. We show that WT RUNX1 is required for survival of t(8;21)-Kasumi-1 and inv(16)-ME-1 AML cell lines. The malignant AML phenotype is sustained by a delicate AML1-ETO/RUNX1 balance that involves competition for common DNA binding sites regulating a subset of AML1-ETO/RUNX1 targets.
Overall design Genomewide sequencing data is included herein: Transcription factors RUNX1 c-terminus and n-terminus which is shared with AML1-ETO were profiled independently), AML1-ETO and AP4 were profiled using ChIP-Seq in Kasumi-1 cells, as well as control ChIP-Seq experiments of non immune serum. Two replicates were performed for each transcription factor profiling and control experiment.
Contributor(s) Ben Ami O, Friedman D
Citation(s) 24055056
Submission date Apr 03, 2013
Last update date May 15, 2019
Contact name Yoram Groner
Organization name Weizmann institute
Department Molecular Genetics
Street address 234 Herzl St.
City Rehovot
ZIP/Postal code 76100
Country Israel
Platforms (1)
GPL10999 Illumina Genome Analyzer IIx (Homo sapiens)
Samples (12)
GSM1113427 Kasumi_RUNX1_1
GSM1113428 Kasumi_RUNX1_2
GSM1113429 Kasumi_AML1_ETO_1
This SubSeries is part of SuperSeries:
GSE45748 Addiction of t(8;21) and inv(16) AML to native RUNX1
BioProject PRJNA196162
SRA SRP020494

Download family Format
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Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE45738_RAW.tar 4.3 Gb (http)(custom) TAR (of BW)
SRA Run SelectorHelp
Raw data are available in SRA
Processed data provided as supplementary file

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