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A Genome-wide Gene Expression Analysis and Database in Transgenic Mice during Development of Amyloid or Tau Pathology

ChEBI2014-12-24 更新2026-07-21 收录

神经退行性机制

转基因小鼠模型

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-64398 数据链接链接失效反馈

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资源简介：

A Genome-wide Gene Expression Analysis and Database in Transgenic Mice during Development of Amyloid or Tau Pathology

应用场景：

创建时间：

2014-12-24

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

Effect of the paternal grandmother of the F2 cross on life span of G59S-hDCTN1 mice.

跨代表观遗传

转基因小鼠模型

Effect of the paternal grandmother of the F2 cross on life span of G59S-hDCTN1 mice.

Figshare2022-09-15 更新10

Enhanced sensitivity of hippocampal pyramidal neurons from mdx mice to hypoxia-induced loss of synaptic transmission.

神经退行性机制

神经元缺氧复氧损伤

The gene at the Duchenne/Becker muscular dystrophy locus encodes dystrophin, a member of a protein superfamily that links the actin cytoskeleton to transmembrane plasmalemmal proteins. In mature skele

PubMed Central1992-03-15 更新00

Differential gene expression in spinal cords from uninfected WT mice and infected RdRP transgenic mice (2 days post infection with Encephalomyocarditis Virus, EMCV)

病毒感染转录组

转基因小鼠模型

Previously, we reported that mice made transgenic for a picornaviral RdRP – the 3Dpol protein of Theiler’s murine encephalomyelitis virus (TMEV) – suppress infection by diverse viral families. How the

NIAID Data Ecosystem30

Table_2_Progressive mitochondrial dysfunction in cerebellar synaptosomes of cystatin B-deficient mice.XLSX

神经退行性机制

线粒体生物能量学

The involvement of mitochondrial dysfunction in cystatin B (CSTB) deficiency has been suggested, but its role in the onset of neurodegeneration, myoclonus, and ataxia in the CSTB-deficient mouse model

NIAID Data Ecosystem10

A Genome-wide Gene Expression Analysis and Database in Transgenic Mice during Development of Amyloid or Tau Pathology

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