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ChIPseq of 15-20 week-old R6/1 HD mice in neuronal and non-neuronal striatal cell populations

ABSTRACT: ChIPseq of 15-20 week-old R6/1 HD mice in neuronal and non-neuronal striatal cell populations

PROVIDER: PRJNA1090131 | ENA |

REPOSITORIES: ENA

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ChIPseq of 15-20 week-old R6/1 HD mice in neuronal and non-neuronal striatal cell populations

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Cut&Tag of 20 week-old HD R6/1 mice in neuronal and non-neuronal striatal cell populations.

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Cut&Tag of 15 week-old HD R6/1 mice in neuronal cell populations.

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Six-week-old R6/2 HD mouse striatum

Project description:Wild-type CBAxC57BL/6 (6 weeks of age) and HD Exon 1 R6/2 CBAxC57BL/6 (6 weeks of age). Control groups for two drug studies. All animals injected with normal saline 30-60 minutes prior to sacrifice. Keywords: parallel sample

2011-10-13 | GSE1980 | GEO

Six-week-old R6/2 HD mouse striatum

2011-10-12 | E-GEOD-1980 | biostudies-arrayexpress

Gene expression data from cortex of 9 week old wild type, R6/2, HDAC4het and R6/2::HDAC4het mice

Project description:Histone deacetylase (HDAC) 4 is a transcriptional repressor that contains a glutamine rich domain. We hypothesised that it may be involved in the molecular pathogenesis of Huntington's disease (HD), a protein folding neurodegenerative disorder caused by an aggregation-prone polyglutamine expansion and transcriptional dysregulation. We found that HDAC4 interacts with huntingtin in a polyglutamine-length dependent manner and co-localises with cytoplasmic inclusions. We show that HDAC4 reduction delayed cytoplasmic aggregate formation, restored Bdnf transcript levels and rescued neuronal and cortico-striatal synaptic function in HD mouse models. This was accompanied by an improvement in motor co-ordination, neurological phenotypes and increased lifespan. Surprisingly, HDAC4 reduction had no effect on global transcriptional dysfunction and did not modulate nuclear huntingtin aggregation. Our results define a crucial role for cytoplasmic aggregation in the molecular pathology of HD. HDAC4 reduction presents a novel strategy for targeting huntingtin aggregation which may be amenable to small molecule therapeutics. mRNA expression analysis was performed by microarray in 9 weeks old WT (n=9), R6/2 (n=9), HDAC4het (n=9) and Double R6/2::HDAC4het (n=10) mice. Microarray quality control was performed using the software package provided on RACE (http://race.unil.ch).

2014-10-10 | E-GEOD-38218 | biostudies-arrayexpress

Gene expression data from cortex of 15 week old wild type, R6/2, HDAC4het and R6/2::HDAC4het mice

Project description:Histone deacetylase (HDAC) 4 is a transcriptional repressor that contains a glutamine rich domain. We hypothesised that it may be involved in the molecular pathogenesis of Huntington's disease (HD), a protein folding neurodegenerative disorder caused by an aggregation-prone polyglutamine expansion and transcriptional dysregulation. We found that HDAC4 interacts with huntingtin in a polyglutamine-length dependent manner and co-localises with cytoplasmic inclusions. We show that HDAC4 reduction delayed cytoplasmic aggregate formation, restored Bdnf transcript levels and rescued neuronal and cortico-striatal synaptic function in HD mouse models. This was accompanied by an improvement in motor co-ordination, neurological phenotypes and increased lifespan. Surprisingly, HDAC4 reduction had no effect on global transcriptional dysfunction and did not modulate nuclear huntingtin aggregation. Our results define a crucial role for cytoplasmic aggregation in the molecular pathology of HD. HDAC4 reduction presents a novel strategy for targeting huntingtin aggregation which may be amenable to small molecule therapeutics. mRNA expression analysis was performed by microarray in 15 weeks old WT (n=8), R6/2 (n=9), HDAC4het (n=8) and Double R6/2::HDAC4het (n=9) mice. Microarray quality control was performed using the software package provided on RACE (http://race.unil.ch).

2014-10-10 | E-GEOD-38219 | biostudies-arrayexpress

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