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Proteomic study of the mechanism of action of mitochondria-targeted tetrahydroxy stilbene glycoside derivatives in APP695V717I transgenic mice

NIAID Data Ecosystem2026-05-01 收录

阿尔茨海默病机制

线粒体靶向蛋白质组学

数据链接：

https://doi.org/10.7910/DVN/HPMUHZ 数据链接链接失效反馈

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资源简介：

This dataset is a proteomic study to investigate the mechanism of action of mitochondria-targeted tetrahydroxystilbene glycoside derivatives in APP695V717I transgenic mice

应用场景：

创建时间：

2024-03-22

阿尔茨海默病机制

神经元基因调控分析

IPA of upstream regulators of genes preferentially expressed in neurons. Table S8 notes the upstream regulators of genes that are downregulated in Alzheimerâ s disease and upregulated by candesartan

Figshare2016-12-16 更新60

Table_1_Protect Effects of Seafood-Derived Plasmalogens Against Amyloid-Beta (1–42) Induced Toxicity via Modulating the Transcripts Related to Endocytosis, Autophagy, Apoptosis, Neurotransmitter Release and Synaptic Transmission in SH-SY5Y Cells.DOC

阿尔茨海默病机制

神经药物靶点

To investigate the underlying mechanisms of decreased plasmalogens (Pls) levels in neurodegenerative diseases, here the effects of seafood-derived Pls on undifferentiated and differentiated human SH-S

NIAID Data Ecosystem50

The CD33 short isoform is a gain-of-function variant that enhances Aß1-42 phagocytosis in microglia I. The CD33 short isoform is a gain-of-function variant that enhances Aß1-42 phagocytosis in microglia I

阿尔茨海默病机制

小胶质细胞吞噬功能

Background: CD33 is genetically linked to Alzheimer’s disease (AD) susceptibility through differential expression of isoforms in microglia. The role of the human CD33 short isoform (hCD33m), preferent

NIAID Data Ecosystem30

CRISPRi Screening of Enhancers in Human Primary Astrocytes Identifies Regulatory Circuitry Disrupted in Alzheimer’s Disease [RNA-seq]

基因调控网络

阿尔茨海默病机制

We used CROP-seq to perform a high-throughput, parallel screen of 979 candidate enhancer perturbations in normal human astrocytes (NHAs), a primary cell-line. We identified the target gene(s) for 145

NIAID Data Ecosystem50

Expression data from the neuron model of Alzheimer's disease (AD) with or without treatment of recombinant human mitochondrial transcriptional factor A (rhTFAM) protein. Homo sapiens

阿尔茨海默病机制

神经退行性疾病基因表达分析

To delineate the mechanism by which hTFAM suppresses AD pathology in the neuron model of AD, we first performed microarray analyses using using RNAs prepared from PS1P117L and wild-type neurons. Next,

NIAID Data Ecosystem30

Proteomic study of the mechanism of action of mitochondria-targeted tetrahydroxy stilbene glycoside derivatives in APP695V717I transgenic mice

资源简介：

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