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Status |
Public on Jul 18, 2013 |
Title |
Targeting H3K4 methylation as a therapeutic strategy for Huntington's disease (ChIP-seq) |
Organism |
Mus musculus |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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Summary |
Transcriptional dysregulation is an early feature of Huntington's disease (HD). We observed gene-specific changes in H3K4me3 at transcriptionally repressed promoters in R6/2 mouse and human HD brain. Genome-wide analysis showed a novel chromatin signature for this mark. Reducing the levels of the H3K4 demethylase SMCX/Jarid1c in primary neurons reversed down-regulation of key neuronal genes caused by mutant Huntingtin (Htt) expression. Finally, reduction of SMCX/Jarid1c in primary neurons from BACHD mice or the single Jarid1 in a Drosophila HD model was protective. Therefore, targeting this epigenetic signature may be an effective strategy to ameliorate the consequences of HD.
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Overall design |
ChIP-seq for H3K4me3 in wild type and R6/2 cortex and striatum at 8 and 12 weeks.
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Contributor(s) |
Ng CW, Yildirim F, Vashishtha M, Gipson T, Thompson LM, Housman D, Fraenkel E |
Citation(s) |
23872847 |
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Submission date |
Jul 17, 2013 |
Last update date |
May 15, 2019 |
Contact name |
Christopher Ng |
Organization name |
Massachusetts Institute of Technology
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Street address |
77 Massachusetts Ave.
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City |
Cambridge |
State/province |
Massachusetts |
ZIP/Postal code |
02139 |
Country |
USA |
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Platforms (2) |
GPL11002 |
Illumina Genome Analyzer IIx (Mus musculus) |
GPL13112 |
Illumina HiSeq 2000 (Mus musculus) |
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Samples (8)
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This SubSeries is part of SuperSeries: |
GSE48963 |
Targeting H3K4 methylation as a therapeutic strategy for Huntington's disease |
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Relations |
BioProject |
PRJNA212433 |
SRA |
SRP027534 |