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Deficits in histone acetylation and methylation are restricted to specific loci in Huntington's disease models

ChEBI2015-12-31 更新2026-07-12 收录

亨廷顿病表观遗传学

组蛋白修饰位点分析

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-63675 数据链接链接失效反馈

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Deficits in histone acetylation and methylation are restricted to specific loci in Huntington's disease models

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创建时间：

2015-12-31

亨廷顿病表观遗传学

DNA甲基化分析

The earliest stages of Huntington’s disease are marked by changes in gene expression that are caused in an indirect and poorly understood manner by polyglutamine expansions in the huntingtin protein (

NIAID Data Ecosystem70

H3K4me3 ChIP-Seq profiles of control and huntington's disease iPSC-derived medium spiny neuron-like cells

亨廷顿病表观遗传学

神经元基因调控

HD and control patient-derived induced pluripotent stem cells were used to generate medium spiny neuron-like cells. Three control in triplicate, one control in duplicate, one HD samples with CAG repe

NIAID Data Ecosystem40

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

亨廷顿病表观遗传学

HTT蛋白染色质结合

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 chromati

NIAID Data Ecosystem30

The top genes with decreased histone H3 acetylation in TG striata.

亨廷顿病表观遗传学

纹状体基因表达分析

Gene symbol annotation for these genes was checked with NCBI's Entrez Gene database (http://www.ncbi.nlm.nih.gov/sites/entrez). In the instances where gene annotation has been updated, we have left th

NIAID Data Ecosystem60

H3K4me3 ChIP-Seq profiles of control and huntington's disease iPSC-derived medium spiny neuron-like cells

亨廷顿病表观遗传学

细胞疾病模型

HD and control patient-derived induced pluripotent stem cells were used to generate medium spiny neuron-like cells. Three control in triplicate, one control in duplicate, one HD samples with CAG repe

NIAID Data Ecosystem30

Deficits in histone acetylation and methylation are restricted to specific loci in Huntington's disease models

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