Increased burden of rare risk variants across gene expression networks predisposes to sporadic Parkinson's disease.

ABSTRACT: Alpha-synuclein (αSyn) is an intrinsically disordered protein that accumulates in the brains of patients with Parkinson's disease and forms intraneuronal inclusions called Lewy Bodies. While the mechanism underlying the dysregulation of αSyn in Parkinson's disease is unclear, it is thought that prionoid cell-to-cell propagation of αSyn has an important role. Through a high throughput screen, we recently identified 38 genes whose knock down modulates αSyn propagation. Follow up experiments were undertaken for two of those genes, TAX1BP1 and ADAMTS19, to study the mechanism with which they regulate αSyn homeostasis. We used a recently developed M17D neuroblastoma cell line expressing triple mutant (E35K+E46K+E61K) "3K" αSyn under doxycycline induction. 3K αSyn spontaneously for

SUBMITTER: Eubanks E 

PROVIDER: S-EPMC11384021 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature