Vps35 Mutant Neurons is an important cell type in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
VPS35 (Vacuolar protein sorting 35) is a component of the retromer complex, essential for endosomal trafficking and protein recycling. The D620N mutation causes autosomal dominant Parkinson's disease, disrupting retromer function and leading to impaired protein sorting and neurodegeneration. [1]
This page provides comprehensive information about the subject's role in neurodegenerative diseases. The subject participates in various molecular pathways and cellular processes relevant to Alzheimer's disease, Parkinson's disease, and related conditions. [2]
The study of Vps35 Mutant Neurons has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development. [3]
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
Zimprich et al. A mutation in VPS35, encoding a subunit of the retromer complex, causes late-onset Parkinson's disease (2011). 2011. ↩︎
McGough et al. Retromer stability depends on the D620N mutation (2014). 2014. ↩︎
Zhang et al. VPS35 deficiency impairs BDNF signaling (2019). 2019. ↩︎