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ATXN2-CAG42 sequesters PABPC1 into insolubility and induces FBXW8 in cerebellum of old ataxic knock-in mice

ChEBI2012-07-24 更新2026-07-21 收录

脊髓小脑性共济失调分子机制

蛋白质稳态失调研究

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-39640 数据链接链接失效反馈

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资源简介：

ATXN2-CAG42 sequesters PABPC1 into insolubility and induces FBXW8 in cerebellum of old ataxic knock-in mice

应用场景：

创建时间：

2012-07-24

神经影像网络分析

脊髓小脑性共济失调分子机制

BackgroundSpinocerebellar ataxia type 3 (SCA3) is a rare movement disorder characterized with ataxia. Previous studies on movement disorders show that the whole-brain functional network tends to be mo

NIAID Data Ecosystem70

The Role of Interruptions in polyQ in the Pathology of SCA1

脊髓小脑性共济失调分子机制

polyQ重复序列分子遗传学

At least nine dominant neurodegenerative diseases are caused by expansion of CAG repeats in coding regions of specific genes that result in abnormal elongation of polyglutamine (polyQ) tracts in the c

Figshare2016-01-18 更新30

Multi-omic profiling reveals the ataxia protein sacsin is required for integrin trafficking and synaptic organization

脊髓小脑性共济失调分子机制

sacsin蛋白功能研究

Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is a childhood-onset cerebellar ataxia caused by mutations in SACS, which encodes the protein sacsin. Cellular ARSACS phenotypes incl

NIAID Data Ecosystem30

Additional file 2: Table S1. of A mutation in the low voltage-gated calcium channel CACNA1G alters the physiological properties of the channel, causing spinocerebellar ataxia

钙通道突变分析

脊髓小脑性共济失调分子机制

Summary of exome sequencing. (XLSX 42Â kb)

Figshare2016-12-15 更新60

Additional file 11: of Transcriptional profiling and biomarker identification reveal tissue specific effects of expanded ataxin-3 in a spinocerebellar ataxia type 3 mouse model

神经退行性疾病生物标志物

脊髓小脑性共济失调分子机制

Blood lipids. (XLSX 82 kb)

Figshare2018-06-22 更新30