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Transcription profiling of rat striatal neuron cultures infected with TRE-Htt-N853 - Huntingtons Disease in vitro model

ABSTRACT: Primary neuron model of Huntington's Disease. 2 treatment groups: A) Infected 4 weeks prior with TRE-Htt-N853-18Q-expressing recombinant lentivirus, B) Infected 4 weeks prior with TRE-Htt-N853-82Q-expressing recombinant lentivirus Experiment Overall Design: Primary neurons samples infected with TRE-Htt-N853-18Q or -82Q.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Alexandre Kuhn

PROVIDER: E-GEOD-12481 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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TRE-Htt-N853 Huntington's Disease in vitro model

Project description:Primary neuron model of Huntington's Disease. 2 treatment groups: A) Infected 4 weeks prior with TRE-Htt-N853-18Q-expressing recombinant lentivirus, B) Infected 4 weeks prior with TRE-Htt-N853-82Q-expressing recombinant lentivirus Keywords: gene expression study

2008-09-01 | GSE12481 | GEO

Htt-N171 HD in vitro

Project description:4 Treatment groups: A) Uninfected B) Infected 6 weeks prior with GFP-expressing recombinant lentivirus C) Infected 6 weeks prior with Htt-N171-19Q-expressing recombinant lentivirus D)Infected 6 weeks prior with Htt-N171-82Q-expressing recombinant lentivirus Keywords = huntington Keywords: parallel sample

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Transcription profiling of rat rat striatal neuron cultures treated with Htt-N171-19Q-expressing recombinant lentivirus

Project description:4 Treatment groups:; A) Uninfected; B) Infected 6 weeks prior with GFP-expressing recombinant lentivirus; C) Infected 6 weeks prior with Htt-N171-19Q-expressing recombinant lentivirus; D)Infected 6 weeks prior with Htt-N171-82Q-expressing recombinant lentivirus

2008-10-25 | E-GEOD-1918 | biostudies-arrayexpress

Effect of IDH1 mutation induced by doxycycline on gene expression during VSVΔ51 infection in LN-229-TRE-R132H glioblastoma cells

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ChIP-seq of HTT protein in mouse cortex following HTT knockdown

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ChIP-seq of HTT protein in mouse cortex following HTT knockdown

Project description:Progressive striatal gene expression changes and epigenetic alterations are a prominent feature of Huntington’s disease (HD), but direct relationships between the huntingtin (HTT) protein and chromatin remain poorly described. Here, using chromatin immunoprecipitation and sequencing (ChIP-seq), we show that HTT reproducibly occupies specific locations in the mouse genome, including thousands of genomic loci that are differentially occupied in striatal tissue from a knock-in mouse model of the HD mutation (B6.HttQ111/+) versus wildtype controls. ChIP-seq of histone modifications, generated in parallel, revealed genotype-specific colocalization of HTT with trimethylation of histone 3 lysine 27 (H3K27me3), a repressive chromatin mark. Near genes that are differentially regulated in HD, greater HTT occupancy in HttQ111/+ vs. wildtype mice predicted increased H3K27me3, reduced histone 3 lysine 4 (H3K4me3), a marker of poised and active promoters, and down-regulated gene expression. Altered huntingtin-chromatin interactions may therefore play a direct role in driving transcriptional dysregulation in HD.

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HTT regulates muscle differentiation in vitro.

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