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Transcription profiling of human cholinergic SN56.B5.G4 cells treated with beta-amyloid or hydrogen peroxide

ChEBI2005-01-01 更新2026-07-21 收录

神经退行性机制

胆碱能神经元转录组

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-MEXP-710 数据链接链接失效反馈

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资源简介：

Transcription profiling of human cholinergic SN56.B5.G4 cells treated with beta-amyloid or hydrogen peroxide

应用场景：

创建时间：

2005-01-01

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

Purkinje neurons with loss of STIM1 exhibit age-dependent changes in gene expression and synaptic components

钙信号调控

神经退行性机制

The Stromal interaction molecule 1 (STIM1) is an ER-Ca2+ sensor and an essential component of ER-Ca2+ store operated Ca2+entry (SOCE). Loss of STIM1 affects metabotropic Glutamate Receptor 1 (mGluR1)

NIAID Data Ecosystem60

Additional file 3 of Single-cell RNA-seq reveals alterations in peripheral CX3CR1 and nonclassical monocytes in familial tauopathy

单细胞转录组学

神经退行性机制

Additional file 3: Table S3. RNA integrity number for PBMC samples.

Figshare2024-09-11 更新40

Misconnecting the dots: altered mitochondrial protein-protein interactions and their role in neurodegenerative disorders

蛋白质相互作用

神经退行性机制

Introduction: Mitochondria (mt) are protein-protein interaction (PPI) hubs in the cell where mt-localized and associated proteins interact in a fashion critical for cell fitness. Altered mtPPIs are li

NIAID Data Ecosystem70

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