ArticleScience advances2025
Alpha-synuclein regulates nucleolar DNA double-strand break repair in melanoma.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Levodopa and Melanoma: Practical Recommendations for Parkinson's Disease-International Parkinson and Movement Disorder Society Scientific Issues Committee Viewpoint.Movement disorders clinical practice · 2026Article
- Deciphering novel genotypic biomarkers and functional alterations in double strand break repair pathways for Parkinson's disease.Scientific reports · 2026Article
- Revisiting the alpha-synuclein paradox in melanoma-Parkinson's disease connection: more than a tale of two cell fates.Cellular and molecular life sciences : CMLS · 2025Review
- Nucleolar aggregation of key neuropathological proteins in the postmortem neurodegenerative brain.Acta neuropathologica · 2025Article
- Transcriptomic analysis of melanoma cells reveals an association of α-synuclein with regulation of the inflammatory response.Scientific reports · 2024Article
- Introducing the Role of Genotoxicity in Neurodegenerative Diseases and Neuropsychiatric Disorders.International journal of molecular sciences · 2024Review
- Polo-like kinase inhibition leads to neuroprotection of neurons bearing alpha-synuclein Lewy body-like inclusionsmicroPublication biology · 2024Article
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15 authors.
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Abstract
Although an increased risk of the skin cancer melanoma in people with Parkinson's disease (PD) has been shown in multiple studies, the mechanisms involved are poorly understood, but increased expression of the PD-associated protein alpha-synuclein (αSyn) in melanoma cells may be important. Our previous work suggests that αSyn can facilitate DNA double-strand break (DSB) repair, promoting genomic stability. We now show that αSyn is preferentially enriched within the nucleolus in melanoma, where it colocalizes with DNA damage markers and DSBs. Inducing DSBs specifically within nucleolar ribosomal DNA (rDNA) increases αSyn levels near sites of damage. αSyn knockout increases DNA damage within the nucleolus at baseline, after specific rDNA DSB induction, and prolongs the rate of recovery from this induced damage. αSyn is important downstream of ataxia-telangiectasia-mutated signaling to facilitate MDC1-mediated 53BP1 recruitment to DSBs, reducing micronuclei formation and promoting cellular proliferation, migration, and invasion.
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