Signaling pathways in skeletal muscle of Amyotrophic Lateral Sclerosis mouse model

ChEBI2014-01-22 更新2026-07-21 收录

神经退行性机制

钙信号通路

数据链接：

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资源简介：

Signaling pathways in skeletal muscle of Amyotrophic Lateral Sclerosis mouse model

创建时间：

2014-01-22

Examination of gene expression in cerebellum and hippocampus for mouse C57BL/6J WT and nmf205-/-

神经退行性机制

细胞应激通路

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Characterization of Inducible Models of Tay-Sachs and Related Disease

GM2神经节苷脂沉积症模型

神经退行性机制

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NIAID Data Ecosystem40

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

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

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