ArticleJournal of neuroscience research2012
Characterization of cellular protective effects of ATP13A2/PARK9 expression and alterations resulting from pathogenic mutants.
Article in Journal of neuroscience research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed.
- Progress in modelling ATP13A2-linked neurodegeneration.NPJ Parkinson's disease · 2026Review
- Clinical Evaluation of Three KRS Families and Cellular Analysis of Distinct ATP13A2 Mutations Reveal Different Levels of Iron Accumulation.Journal of neurochemistry · 2026Article
- ATP13A2 restrains macrophage NLRP3 inflammasome activation to repress neurodegeneration via modulating mitochondrial homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Genetic heterogeneity in epilepsy and comorbidities: insights from Pakistani families.BMC neurology · 2024Article
- Unveiling the molecular complexity of proliferative diabetic retinopathy through scRNA-seq, AlphaFold 2, and machine learning.Frontiers in endocrinology · 2024Article
- ATP13A2 Gene Silencing in Drosophila Affects Autophagic Degradation of A53T Mutant α-Synuclein.International journal of molecular sciences · 2023Article
- ATP13A2 (PARK9) and basal ganglia function.Frontiers in neurology · 2023Review
- Review
- The Roles ofFrontiers in cellular neuroscience · 2022Review
- Review
- Manganese Accumulation in the Brain via Various Transporters and Its Neurotoxicity Mechanisms.Molecules (Basel, Switzerland) · 2020Review
- The Role of Oxidative Stress in Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2020Review
- Article
- Dysregulated Interorganellar Crosstalk of Mitochondria in the Pathogenesis of Parkinson's Disease.Cells · 2020Review
- The effect of manganese exposure in Atp13a2-deficient mice.Neurotoxicology · 2018Article
- Article
- Mechanisms of Gene-Environment Interactions in Parkinson's Disease.Current environmental health reports · 2017Review
- Loss-of-function mutations in the ATP13A2/PARK9 gene cause complicated hereditary spastic paraplegia (SPG78).Brain : a journal of neurology · 2017Article
- The Central Role of Biometals Maintains Oxidative Balance in the Context of Metabolic and Neurodegenerative Disorders.Oxidative medicine and cellular longevity · 2017Review
- Using the social amoeba Dictyostelium to study the functions of proteins linked to neuronal ceroid lipofuscinosis.Journal of biomedical science · 2016Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Mutations in ATP13A2, which encodes a lysosomal P-type ATPase of unknown function, cause an autosomal recessive parkinsonian syndrome. With mammalian cells, we show that ATP13A2 expression protects against manganese and nickel toxicity, in addition to proteasomal, mitochondrial, and oxidative stress. Consistent with a recessive mode of inheritance of gene defects, disease-causing mutations F182L and G504R are prone to misfolding and do not protect against manganese and nickel toxicity because they are unstable as a result of degradation via the endoplasmic reticulum-associated degradation (ERAD)-proteasome system. The protective effects of ATP13A2 expression are not due to inhibition of apoptotic pathways or a reduction in typical stress pathways, insofar as these pathways are still activated in challenged ATP13A2-expressing cells; however, these cells display a dramatic reduction in the accumulation of oxidized and damaged proteins. These data indicate that, contrary to a previous suggestion, ATP13A2 is unlikely to convey cellular resilience simply by acting as a lysosomal manganese transporter. Consistent with the recent identification of an ATP13A2 recessive mutation in Tibetan terriers that develop neurodegeneration with neuronal ceroid lipofucinoses, our data suggest that ATP13A2 may function to import a cofactor required for the function of a lysosome enzyme(s).
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Registered trials
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