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Divergent impacts of C9orf72 repeat expansion on neurons and glia in ALS and FTD

NIAID Data Ecosystem2026-05-01 收录

神经退行性机制

C9orf72基因病理学

数据链接：

https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE219281 数据链接链接失效反馈

官方服务：

资源简介：

This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

应用场景：

创建时间：

2023-09-27

神经退行性机制

细胞应激通路

Ribosome stalling during translation has recently been shown to cause neurodegeneration, yet the signaling pathways triggered by stalled elongation complexes are unknown. To investigate these pathw

NIAID Data Ecosystem100

Loss of TREM2 reduces hyperactivation of progranulin deficient microglia but not lysosomal pathology [14 months]

神经退行性机制

胶质细胞功能研究

GRN haploinsufficiency causes frontotemporal lobar degeneration and results in microglial hyperactivation, lysosomal dysfunction and TDP-43 deposition. To understand the contribution of microglial hyp

NIAID Data Ecosystem30

MOESM7 of Unique molecular signature in mucolipidosis type IV microglia

神经退行性机制

胶质细胞转录组学

Additional file 7: Table S3. raw data used to build Fig. 4a with expression as log2 fold change vs. controls.

Figshare2019-12-28 更新20

AAGGG repeat expansions trigger RFC1-independent synaptic dysregulation in human CANVAS Neurons. AAGGG repeat expansions trigger RFC1-independent synaptic dysregulation in human CANVAS Neurons

神经退行性机制

功能障碍研究

This SuperSeries is composed of the SubSeries listed below. Overall design: Refer to individual Series

NIAID Data Ecosystem40

Additional file 15 of Comparative analysis of transcriptome remodeling in plaque-associated and plaque-distant microglia during amyloid-β pathology progression in mice