ArticleEMBO reports2023
Dynamic reversibility of α-synuclein serine-129 phosphorylation is impaired in synucleinopathy models.
Article in EMBO reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 20 citations in OpenAlex.
- Dual effect of α-synuclein disease variants on condensate formation.Nature communications · 2026Article
- Quantifying the Acute Toxicity of Alpha-Synuclein Membrane-Accumulation in a Cell-Based Assay.Journal of molecular neuroscience : MN · 2026Article
- Lipid droplets promote aberrant liquid-liquid phase separation of alpha-synuclein impairing energy homeostasis.EMBO reports · 2026Article
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- Authentic Phosphorylation of α-Synuclein at Ser129 Reveals Functional Differences Not Captured by the S129D Phosphomimetic.ACS chemical biology · 2026Article
- Targeting of kinases to treat neurodegenerative diseases.Pharmacological reviews · 2026Review
- Antiviral innate immunity induces alpha synuclein phosphorylation at serine129 in neurons independent of aggregation.NPJ Parkinson's disease · 2026Article
- A Novel α-Synuclein K58N Missense Variant in a Patient with Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2025Article
- A novel alpha-synuclein G14R missense variant is associated with atypical neuropathological features.Molecular neurodegeneration · 2025Article
- Increased burden of rare risk variants across gene expression networks predisposes to sporadic Parkinson's disease.Cell reports · 2025Article
- A novel alpha-synuclein K58N missense variant in a patient with Parkinson's disease.medRxiv : the preprint server for health sciences · 2025Article
- Parkinson disease-associated toxic exposures selectively up-regulate vesicular glutamate transporter vGlut2 in a model of human cortical neurons.Molecular biology of the cell · 2025Article
- Alpha synuclein and inflammaging.Heliyon · 2025Review
- Acute lipid droplet accumulation induced by the inhibition of the phospholipase DDHD2 does not affect the level, solubility, or phosphoserine-129 status of α-synuclein.Metabolic brain disease · 2025Article
- Physiological roles of α-synuclein serine-129 phosphorylation - not an oxymoron.Trends in neurosciences · 2024Review
- Alpha-synuclein aggregates are phosphatase resistant.Acta neuropathologica communications · 2024Article
- Alpha-synuclein aggregates are phosphatase resistant.bioRxiv : the preprint server for biology · 2024Article
- Dynamic reversibility of α-synuclein serine-129 phosphorylation is impaired in synucleinopathy models.EMBO reports · 2023Article
- α-Synuclein serine129 phosphorylation - the physiology of pathology.Molecular neurodegeneration · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
α-Synuclein phosphorylation at serine-129 (pS129) is a widely used surrogate marker of pathology in Parkinson's disease and other synucleinopathies. However, we recently demonstrated that phosphorylation of S129 is also a physiological activator of synaptic transmission. In a feed-forward fashion, neuronal activity triggers reversible pS129. Here, we show that Parkinson's disease-linked missense mutations in SNCA impact activity-dependent pS129. Under basal conditions, cytosol-enriched A30P, H50Q, and G51D mutant forms of α-synuclein exhibit reduced pS129 levels in rat primary cortical neurons. A53T pS129 levels are similar to wild-type, and E46K pS129 levels are higher. A30P and E46K mutants show impaired reversibility of pS129 after stimulation. For the engineered profoundly membrane-associated α-synuclein mutant "3K" (E35K + E46K + E61K), de-phosphorylation was virtually absent after blocking stimulation, implying that reversible pS129 is severely compromised. Importantly, pS129 excess resulting from proteasome inhibition is also associated with reduced reversibility by neuronal inhibition, kinase inhibition, or phosphatase activation. Our findings suggest that perturbed pS129 dynamics are probably a shared characteristic of pathology-associated α-synuclein, with possible implications for synucleinopathy treatment and diagnosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.