ArticleLife science alliance2019
Mechanistic insights into the protective roles of polyphosphate against amyloid cytotoxicity.
Article in Life science alliance, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- Review
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- From Food Additives to Neurodegeneration: The Emerging Role of Polyphosphates in Tauopathies.ACS chemical neuroscience · 2026Review
- Review
- A systematic study of regulating inorganic polyphosphates production inSynthetic and systems biotechnology · 2025Article
- Inorganic Polyphosphate: An Emerging Regulator of Neuronal Bioenergetics and Its Implications in Neuroprotection.Biomolecules · 2025Review
- Polyphosphate: a cellular Swiss army knife.Current opinion in biotechnology · 2025Review
- Optical signature of retinal Tau fibrillation.Scientific reports · 2025Article
- Short-term starvation activates AMPK and restores mitochondrial inorganic polyphosphate, but fails to reverse associated neuronal senescence.Aging cell · 2024Article
- Amyloid accelerator polyphosphate fits as the mystery density in α-synuclein fibrils.PLoS biology · 2024Article
- The Protein Scaffolding Functions of Polyphosphate.Journal of molecular biology · 2024Review
- Importance of Non-Covalent Interactions in Yeast Cell Wall Molecular Organization.International journal of molecular sciences · 2024Review
- Causation in neuroscience: keeping mechanism meaningful.Nature reviews. Neuroscience · 2024Review
- Mitochondrial inorganic polyphosphate is required to maintain proteostasis within the organelle.Frontiers in cell and developmental biology · 2024Article
- Enzymatic Depletion of Mitochondrial Inorganic Polyphosphate (polyP) Increases the Generation of Reactive Oxygen Species (ROS) and the Activity of the Pentose Phosphate Pathway (PPP) in Mammalian Cells.Antioxidants (Basel, Switzerland) · 2022Article
- Polyphosphate in Antiviral Protection: A Polyanionic Inorganic Polymer in the Fight Against Coronavirus SARS-CoV-2 Infection.Progress in molecular and subcellular biology · 2022Article
- Polyphosphate drives bacterial heterochromatin formation.Science advances · 2021Article
- Depletion of mitochondrial inorganic polyphosphate (polyP) in mammalian cells causes metabolic shift from oxidative phosphorylation to glycolysis.The Biochemical journal · 2021Article
- Is there a link between inorganic polyphosphate (polyP), mitochondria, and neurodegeneration?Pharmacological research · 2021Review
- Regulation of Functional Protein Aggregation by Multiple Factors: Implications for the Amyloidogenic Behavior of the CAP Superfamily Proteins.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
The universally abundant polyphosphate (polyP) accelerates fibril formation of disease-related amyloids and protects against amyloid cytotoxicity. To gain insights into the mechanism(s) by which polyP exerts these effects, we focused on α-synuclein, a well-studied amyloid protein, which constitutes the major component of Lewy bodies found in Parkinson's disease. Here, we demonstrate that polyP is unable to accelerate the rate-limiting step of α-synuclein fibril formation but effectively nucleates fibril assembly once α-synuclein oligomers are formed. Binding of polyP to α-synuclein either during fibril formation or upon fibril maturation substantially alters fibril morphology and effectively reduces the ability of α-synuclein fibrils to interact with cell membranes. The effect of polyP appears to be α-synuclein fibril specific and successfully prevents the uptake of fibrils into neuronal cells. These results suggest that altering the polyP levels in the extracellular space might be a potential therapeutic strategy to prevent the spreading of the disease.
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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.