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Nrf2-related oxidative stress response and impaired dopamine biosynthesis in a PC12 cell model of Huntingtonâs disease

ChEBI2010-06-25 更新2026-07-21 收录

神经退行性机制

细胞模型病理研究

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https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-10581 数据链接链接失效反馈

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Nrf2-related oxidative stress response and impaired dopamine biosynthesis in a PC12 cell model of Huntingtonâs disease

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2010-06-25

神经退行性机制

细胞应激通路

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Loss of TREM2 reduces hyperactivation of progranulin deficient microglia but not lysosomal pathology [14 months]

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胶质细胞功能研究

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Additional file 15 of Comparative analysis of transcriptome remodeling in plaque-associated and plaque-distant microglia during amyloid-β pathology progression in mice

神经退行性机制

胶质细胞转录组学

Additional file 15: Table S3. Expression values for all expressed genes (in pseudocounts), related to Fig. 2.

Figshare2022-09-26 更新20

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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Fecal microbiota transplantation derived from Alzheimer's disease mice worsens brain trauma outcomes in young C57BL/6 mice

神经退行性机制

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Traumatic brain injury causes neuroinflammation and neurodegeneration, which increase the risk and accelerate the progression of Alzheimer disease. The gut microbiome is an essential modulator of the

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Nrf2-related oxidative stress response and impaired dopamine biosynthesis in a PC12 cell model of Huntingtonâs disease

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Nrf2-related oxidative stress response and impaired dopamine biosynthesis in a PC12 cell model of Huntingtonâs disease