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Status |
Public on Feb 14, 2020 |
Title |
Paired ChIP-Seq studies of Kasumi-1 t(8;21) AML cells |
Organism |
Homo sapiens |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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Summary |
Nearly 10-15% of all acute myeloid leukemia (AML) cases are caused by a recurring chromosomal translocation between 8 and 21, t(8;21). The t(8;21) translocation generates the AML1-ETO leukemia fusion protein. AML1-ETO promotes leukemogenesis by transcriptionally dysregulating important cell-fate genes. Here, to better understand how AML1-ETO deregulates transcription, we performed paired ChIP-Seq analyses of sequence-specific transcription factors, coactivators, corepressors, HDACs, RNA Pol II and acetyl-histone marks in both control and AML1-ETO-depleted Kasumi-1 t(8;21) AML cells.
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Overall design |
Chromatin immunoprecipitation using specific antibodies followed by deep sequencing in Kasumi-1 t(8;21) AML cells.
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Contributor(s) |
Zhang J |
Citation(s) |
32071087 |
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Submission date |
May 29, 2019 |
Last update date |
May 15, 2020 |
Contact name |
Jinsong Zhang |
E-mail(s) |
jinsongzhang@slu.edu
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Phone |
(314)977-6496
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Organization name |
Saint Louis University School of Medicine
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Department |
Department of Pharmacology & Physiology
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Street address |
1402 South Grand Blvd.
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City |
St. Louis |
State/province |
MO |
ZIP/Postal code |
63104 |
Country |
USA |
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Platforms (1) |
GPL16791 |
Illumina HiSeq 2500 (Homo sapiens) |
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Samples (26)
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Relations |
BioProject |
PRJNA545353 |
SRA |
SRP199800 |