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Series GSE104745 Query DataSets for GSE104745
Status Public on Oct 11, 2017
Title Brd4 and CEBPB binding profiles with or without BET inhibitor JQ1 in human leukemia OCI-AML3 cells
Organism Homo sapiens
Experiment type Genome binding/occupancy profiling by high throughput sequencing
Summary Brd4 is the best characterized member of the bromo- and extra-terminal (BET) domain family of proteins and has been widely studied in tumor-associated transcriptional programs. Here we show that activation of Brd4 is associated with the presence of autophagy in NPMc+ and MLL AML cells. Brd4 binds to the promoters of Atg 3, 7 and CEBPb, and expression of these genes is markedly reduced by inhibitors of Brd4, as well as by Brd4-shRNA and CEBPb depletion. Inhibitors of Brd4 also dramatically suppress the transcription of Keap1, thereby increasing the expression of anti-oxidant genes through the Nrf2 pathway. We conclude that Brd4 plays a significant role in autophagy activation through the direct transcriptional regulation of genes essential for autophagy, as well as through the Keap1-Nrf2 axis in NPMc+ and MLL-fusion AML cells.
Overall design Chromatin immunoprecipitation of Brd4 and CEBPB followed by high-throughput sequencing (ChIP-seq) in human NPMc+ leukemia OCI-AML3 cells in the presence or absence of BET inhibitor JQ1.
Contributor(s) Huang M, Mitchell BS
Citation(s) 29545928
Submission date Oct 10, 2017
Last update date May 15, 2019
Contact name Min Huang
Organization name Stanford Cancer Institute
Department Internal Medicine
Lab Beverly Mitchell
Street address 265 Campus Drive
City Stanford
State/province CA
ZIP/Postal code 94305
Country USA
Platforms (1)
GPL11154 Illumina HiSeq 2000 (Homo sapiens)
Samples (6)
GSM2807116 Brd4-CHIP-control
GSM2807117 Brd4-CHIP-JQ1
GSM2807118 CEBPB-CHIP-control
BioProject PRJNA413745
SRA SRP119635

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Supplementary file Size Download File type/resource
GSE104745_RAW.tar 1.7 Gb (http)(custom) TAR (of BIGWIG)
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Raw data are available in SRA
Processed data provided as supplementary file

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