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NPGPx-mediated adaptation to oxidative stress by directly modulating O-GlcNAcase protects motor neuron from degeneration in aging

Mendeley Data2019-06-29 更新2026-04-09 收录

神经退行性机制

氧化应激分子通路

数据链接：

https://data.mendeley.com/datasets/3jgtsc7fbn 数据链接链接失效反馈

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资源简介：

Tiff figures for Immunoprecipitation and Western Blot analysis

应用场景：

创建时间：

2019-06-29

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

Bassoon proteinopathy drives neurodegeneration in multiple sclerosis

神经退行性机制

蛋白质病理沉积

During the course of multiple sclerosis (MS), inflammatory insults drive neuro-axonal loss and disability progression. However, pathways that guide neurons toward survival or death during central nerv

NIAID Data Ecosystem30

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