ArticleCell death and differentiation2013
The Ca2+/Mn2+ ion-pump PMR1 links elevation of cytosolic Ca(2+) levels to α-synuclein toxicity in Parkinson's disease models.
Article in Cell death and differentiation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 75 citations in OpenAlex.
- Proteostasis of organelles in aging and disease.The FEBS journal · 2026Review
- The cross-linking activity of transglutaminase 2 drives α-Synuclein pathology in synucleinopathy models.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Drug discovery and development for Parkinson's disease: are preclinical models good enough?Frontiers in aging neuroscience · 2025Review
- Shedding Light on Calcium Dynamics in the Budding Yeast: A Review on Calcium Monitoring with Recombinant Aequorin.Molecules (Basel, Switzerland) · 2024Review
- Neuroinflammation and Dyskinesia: A Possible Causative Relationship?Brain sciences · 2024Review
- The Role of Calcium and Iron Homeostasis in Parkinson's Disease.Brain sciences · 2024Review
- Mitochondrial Calcium Transport During Autophagy Initiation.Mitochondrial communications · 2024Article
- A mitochondrial inside-out iron-calcium signal reveals drug targets for Parkinson's disease.Cell reports · 2023Article
- Dysregulation of astrocytic CaActa neuropathologica · 2023Article
- Harnessing IGF-1 and IL-2 as biomarkers for calcineurin activity to tailor optimal FK506 dosage in α-synucleinopathies.Frontiers in molecular biosciences · 2023Article
- Cholecalciferol (VD3) Attenuates L-DOPA-Induced Dyskinesia in Parkinsonian Mice Via Modulation of Microglia and Oxido-Inflammatory Mechanisms.Nigerian journal of physiological sciences : official publication of the Physiological Society of Nigeria · 2022Article
- Gastric Enteric Glial Cells: A New Contributor to the Synucleinopathies in the MPTP-Induced Parkinsonism Mouse.Molecules (Basel, Switzerland) · 2022Article
- Sleep-controlling neurons are sensitive and vulnerable to multiple forms of α-synuclein: implications for the early appearance of sleeping disorders in α-synucleinopathies.Cellular and molecular life sciences : CMLS · 2022Article
- Linking α-synuclein-induced synaptopathy and neural network dysfunction in early Parkinson's disease.Brain communications · 2022Review
- Ca2+ administration prevents α-synuclein proteotoxicity by stimulating calcineurin-dependent lysosomal proteolysis.PLoS genetics · 2021Article
- Neurons and Glia Interplay in α-Synucleinopathies.International journal of molecular sciences · 2021Review
- Apoptosis, Induced by Human α-Synuclein in Yeast, Can Occur Independent of Functional Mitochondria.Cells · 2020Article
- Review
- DNA Methyltransferase 1 (DNMT1) Acts on Neurodegeneration by Modulating Proteostasis-Relevant Intracellular Processes.International journal of molecular sciences · 2020Article
- Primary Active CaCold Spring Harbor perspectives in biology · 2020Review
Corrections and comments
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Authors and funding
22 authors at 6 institutions in 6 countries.
Funding
Abstract
Parkinson's disease (PD) is characterized by the progressive loss of dopaminergic neurons, which arises from a yet elusive concurrence between genetic and environmental factors. The protein α-synuclein (αSyn), the principle toxic effector in PD, has been shown to interfere with neuronal Ca(2+) fluxes, arguing for an involvement of deregulated Ca(2+) homeostasis in this neuronal demise. Here, we identify the Golgi-resident Ca(2+)/Mn(2+) ATPase PMR1 (plasma membrane-related Ca(2+)-ATPase 1) as a phylogenetically conserved mediator of αSyn-driven changes in Ca(2+) homeostasis and cytotoxicity. Expression of αSyn in yeast resulted in elevated cytosolic Ca(2+) levels and increased cell death, both of which could be inhibited by deletion of PMR1. Accordingly, absence of PMR1 prevented αSyn-induced loss of dopaminergic neurons in nematodes and flies. In addition, αSyn failed to compromise locomotion and survival of flies when PMR1 was absent. In conclusion, the αSyn-driven rise of cytosolic Ca(2+) levels is pivotal for its cytotoxicity and requires PMR1.
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