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Status |
Public on Jan 31, 2013 |
Title |
H3K4 demethylation by Jarid1a and Jarid1b contributes to retinoblastoma-mediated gene silencing during cellular senescence (ChIP-seq) |
Organism |
Homo sapiens |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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Summary |
Cellular senescence is a tumor-suppressive program that involves chromatin reorganization and specific changes in gene expression that trigger an irreversible cell-cycle arrest. We combined quantitative mass spectrometry and ChIP deep-sequencing to identify changes in histone modification occurring during cellular senescence.
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Overall design |
ChIP-seq was carried out using H3K4me3-specific antibodies in growing, quiescent, senescent, or senescent with shRB targeting Rb, IMR90 cells. The control mock data (ChIP-seq using anti-mouse IgG antibody) is available in GEO Sample GSM497500 (Series GSE19898).
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Contributor(s) |
Chicas A, Lowe SW, Wang X |
Citation(s) |
22615382 |
Submission date |
Jan 30, 2013 |
Last update date |
May 15, 2019 |
Contact name |
Agustin Chicas |
E-mail(s) |
agustin_chicas@H3biomedicine.com
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Organization name |
Memorial Sloan Kettering
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Street address |
One Bungtown Road
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City |
Cold Spring Harbor |
State/province |
NY |
ZIP/Postal code |
11724 |
Country |
USA |
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Platforms (1) |
GPL9052 |
Illumina Genome Analyzer (Homo sapiens) |
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Samples (4)
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This SubSeries is part of SuperSeries: |
GSE43922 |
H3K4 demethylation by Jarid1a and Jarid1b contributes to retinoblastoma-mediated gene silencing during cellular senescence |
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Relations |
BioProject |
PRJNA188187 |
SRA |
SRP018313 |