ArticleThe FEBS journal2009
Parkin deficiency disrupts calcium homeostasis by modulating phospholipase C signalling.
Article in The FEBS journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 50 citations in OpenAlex.
- Mitochondrial CaAntioxidants (Basel, Switzerland) · 2026Article
- Formation of seeding-competent α-synuclein aggregates in parkin-deficient iPSC-derived human neurons.NPJ Parkinson's disease · 2025Article
- Calcium-mediated regulation of mitophagy: implications in neurodegenerative diseases.npj metabolic health and disease · 2025Review
- Linking Heat Shock Protein 70 and Parkin in Parkinson's Disease.Molecular neurobiology · 2023Review
- PINK1 and Parkin regulate IPNature communications · 2023Article
- Post-translational modification and mitochondrial function in Parkinson's disease.Frontiers in molecular neuroscience · 2023Review
- Mitophagy, a Form of Selective Autophagy, Plays an Essential Role in Mitochondrial Dynamics of Parkinson's Disease.Cellular and molecular neurobiology · 2022Review
- Parkin as a Molecular Bridge Linking Alzheimer's and Parkinson's Diseases?Biomolecules · 2022Review
- Resveratrol Treatment in HumanBiomolecules · 2021Article
- PINK1/Parkin Mediated Mitophagy, CaInternational journal of molecular sciences · 2020Review
- Exosomes from Human Periapical Cyst-MSCs: Theranostic Application in Parkinson's Disease.International journal of medical sciences · 2020Review
- Parkin Mutation Affects Clock Gene-Dependent Energy Metabolism.International journal of molecular sciences · 2019Article
- Increased Levels of cAMP by the Calcium-Dependent Activation of Soluble Adenylyl Cyclase inCells · 2019Article
- Parkin in Parkinson's Disease and Cancer: a Double-Edged Sword.Molecular neurobiology · 2018Review
- Current perspective of mitochondrial biology in Parkinson's disease.Neurochemistry international · 2018Review
- Haplotype-specific MAPT exon 3 expression regulated by common intronic polymorphisms associated with Parkinsonian disorders.Molecular neurodegeneration · 2017Article
- Ceramide induced mitophagy and tumor suppression.Biochimica et biophysica acta · 2015Review
- Mitochondrial contagion induced by Parkin deficiency in Drosophila hearts and its containment by suppressing mitofusin.Circulation research · 2014Article
- The mitochondrial chaperone protein TRAP1 mitigates α-Synuclein toxicity.PLoS genetics · 2012Article
- Macroautophagy-generated increase of lysosomal amyloid β-protein mediates oxidant-induced apoptosis of cultured neuroblastoma cells.Autophagy · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Mutations in the E3 ubiquitin ligase parkin cause early-onset, autosomal-recessive juvenile parkinsonism (AJRP), presumably as a result of a lack of function that alters the level, activity, aggregation or localization of its substrates. Recently, we have reported that phospholipase Cgamma1 is a substrate for parkin. In this article, we show that parkin mutants and siRNA parkin knockdown cells possess enhanced levels of phospholipase Cgamma1 phosphorylation, basal phosphoinositide hydrolysis and intracellular Ca2+ concentration. The protein levels of Ca2+-regulated protein kinase Calpha were decreased in AJRP parkin mutant cells. Neomycin and dantrolene both decreased the intracellular Ca2+ levels in parkin mutants in comparison with those seen in wild-type parkin cells, suggesting that the differences were a consequence of altered phospholipase C activity. The protection of wild-type parkin against 6-hydroxydopamine (6OHDA) toxicity was also established in ARJP mutants on pretreatment with dantrolene, implying that a balancing Ca2+ release from ryanodine-sensitive stores decreases the toxic effects of 6OHDA. Our findings suggest that parkin is an important factor for maintaining Ca2+ homeostasis and that parkin deficiency leads to a phospholipase C-dependent increase in intracellular Ca2+ levels, which make cells more vulnerable to neurotoxins, such as 6OHDA.
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Identifiers
What OpenQuestion holds
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.