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The Role of SQSTM1 (P62) in Mitochondrial Function and Clearance in Human Cortical Neurons

ChEBI2021-01-18 更新2026-07-12 收录

神经细胞自噬

神经退行性机制

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-MTAB-9383 数据链接链接失效反馈

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资源简介：

The Role of SQSTM1 (P62) in Mitochondrial Function and Clearance in Human Cortical Neurons

应用场景：

创建时间：

2021-01-18

神经退行性机制

细胞应激通路

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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)

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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

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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

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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

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