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Variable glutamine-rich repeats modulate the function of the transcriptional regulator SSN6

Alliance of Genome Resources2026-08-01 收录

神经退行性机制

谷氨酰胺重复序列扩增

数据链接：

https://www.yeastgenome.org/dataset/GSE70209 数据链接链接失效反馈

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资源简介：

Excessive expansions of glutamine (Q)-rich repeats in various human proteins are known to result in severe neurodegenerative disorders such as Huntington’s disease and several ataxias

应用场景：

网络药理学

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Determining transcriptome changes in whole spinal cord of GarsdelETAQ/+ adult onset mice [18-burgess-006]

神经退行性机制

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To determine transcriptome changes in spinal cord induced by the GarsdelETAQ mutation. How mutations in broadly expressed housekeeping genes lead to neurodegeneration in specific cell types remains un

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The TREM2-APOE pathway drives the transcriptional phenotype of dysfunctional microglia in neurodegenerative diseases V

神经退行性机制

小胶质细胞表型

Microglia play a pivotal role in the maintenance of brain homeostasis, but lose their homeostatic function during the course of neurodegenerative disorders. We identified a specific APOE-dependent mol

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Type I Interferon Signaling Mediates Microglial Dysfunction and Senescence in Human-Mouse Chimeric Brain Models of Down Syndrome and Alzheimer's Disease [single-cell RNA-seq]

神经退行性机制

小胶质细胞衰老

Microglia are critical for brain development and play a central role in Alzheimer's disease (AD) etiology. Down syndrome (DS), also known as trisomy 21, is the most common genetic origin of intellectu

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APOE3-R136S mutation confers resilience against tau pathology via cGAS-STING-IFN inhibition [bulk RNA-seq]

神经退行性机制

胶质细胞转录组学

The Christchurch mutation (R136S) on the APOE3 (E3S/S) gene is associated with attenuation of tau load and cognitive decline despite the presence of a causal PSEN1 mutation and high levels of amyloid

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Variable glutamine-rich repeats modulate the function of the transcriptional regulator SSN6

资源简介：

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