E-GEOD-48960 - Targeting H3K4 methylation as a therapeutic strategy for Huntington's disease (ChIP-seq)

Released on 18 July 2013, last updated on 3 May 2014
Mus musculus
Samples (8)
Protocols (2)
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. ChIP-seq for H3K4me3 in wild type and R6/2 cortex and striatum at 8 and 12 weeks.
Experiment type
Christopher Ng <geo@ncbi.nlm.nih.gov>, Christopher W Ng, David Housman, Ernest Fraenkel, Ferah Yildirim, Leslie M Thompson, Malini Vashishtha, Theresa Gipson
Targeting H3K4 trimethylation in Huntington disease. Vashishtha M, Ng CW, Yildirim F, Gipson TA, Kratter IH, Bodai L, Song W, Lau A, Labadorf A, Vogel-Ciernia A, Troncosco J, Ross CA, Bates GP, Krainc D, Sadri-Vakili G, Finkbeiner S, Marsh JL, Housman DE, Fraenkel E, Thompson LM. , Europe PMC 23872847
Exp. designProtocolsVariablesProcessedSeq. reads