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Status |
Public on Mar 30, 2015 |
Title |
DOT1L Inhibits SIRT1 and SUV39H1-Mediated H3K9 Modification to Maintain Gene Expression [ChIP-seq 2] |
Organism |
Homo sapiens |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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Summary |
Methylation of histone 3 on lysine 79 (H3K79) is broadly associated with active gene expression in eukaryotes, and the H3K79 methyltransferase DOT1L is indispensable for specific leukemia subtypes like those with MLL-translocations. We found that suppression of the histone deacetylase SIRT1 rescued MLL-AF9 leukemia cells from their dependence on DOT1L. We show that upon DOT1L inhibition, SIRT1 is required for the acquisition of a repressive chromatin state consistent with facultative heterochromatin around MLL-AF9 target genes in leukemia and other genes possess an H3K79me2(hi), H3K9ac(hi), H3K9me2(low) histone modification profile in normal hematopoietic stem and progenitor cells.
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Overall design |
Examination of histone modifications via ChIP-seq in three human cancer cell lines.
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Contributor(s) |
Koche RP, Chen CW, Armstrong SA |
Citation missing |
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Submission date |
Oct 06, 2014 |
Last update date |
May 15, 2019 |
Contact name |
Richard Koche |
E-mail(s) |
kocher@mskcc.org
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Organization name |
Memorial Sloan Kettering Cancer Center
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Street address |
417 E. 68th St.
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City |
New York |
State/province |
New York |
ZIP/Postal code |
10065 |
Country |
USA |
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Platforms (1) |
GPL14761 |
Helicos HeliScope (Homo sapiens) |
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Samples (6)
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This SubSeries is part of SuperSeries: |
GSE61022 |
DOT1L Inhibits SIRT1 and SUV39H1-Mediated H3K9 Modification to Maintain Gene Expression |
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Relations |
BioProject |
PRJNA263192 |
SRA |
SRP048679 |