ArticleThe EMBO journal2013
Endonuclease G mediates α-synuclein cytotoxicity during Parkinson's disease.
Article in The EMBO journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
55 citing papers in PubMed, 82 citations in OpenAlex.
- Single-Nucleotide Polymorphisms in Genes Associated with Mitochondrial and DNA Damage Response Modulate the Risk of Non-Alcoholic Fatty Liver Disease in Humans.International journal of molecular sciences · 2026Article
- An engineered viral RNA degrader on mitochondrial surface that mitigates RNA virus infection.Nature communications · 2026Article
- EOR-1/PLZF promotes WAH-1/AIF-dependent compartment-specific corpse clearance.Cell death discovery · 2025Article
- Endonuclease G promotes hepatic mitochondrial respiration by selectively increasing mitochondrial tRNAProceedings of the National Academy of Sciences of the United States of America · 2025Article
- A Brief Review on Caenorhabditis elegans Role in Modelling Neurodegenerative Disease.Central nervous system agents in medicinal chemistry · 2025Review
- Probing the importance of AIF interaction with endonuclease G in mitochondrial inheritance and neurodegeneration.Cell discovery · 2024Article
- The Activity of YCA1 Metacaspase Is Regulated by Reactive Sulfane Sulfur via Persulfidation inAntioxidants (Basel, Switzerland) · 2024Article
- Article
- Apoptotic Factors Are Evolutionarily Conserved Since Mitochondrial Domestication.Genome biology and evolution · 2023Article
- Cytoplasmic Endonuclease G promotes nonalcoholic fatty liver disease via mTORC2-AKT-ACLY and endoplasmic reticulum stress.Nature communications · 2023Article
- Single-Nucleotide Polymorphisms in Genes Maintaining the Stability of Mitochondrial DNA Affect the Occurrence, Onset, Severity and Treatment of Major Depressive Disorder.International journal of molecular sciences · 2023Article
- Nuclear endonuclease G controls cell proliferation in ovarian cancer.FEBS open bio · 2023Article
- Review
- Yca1 metacaspase: diverse functions determine how yeast live and let die.FEMS yeast research · 2023Article
- The HSP40 chaperone Ydj1 drives amyloid beta 42 toxicity.EMBO molecular medicine · 2022Article
- Karyopherin abnormalities in neurodegenerative proteinopathies.Brain : a journal of neurology · 2021Review
- Autophagy restricts mitochondrial DNA damage-induced release of ENDOG (endonuclease G) to regulate genome stability.Autophagy · 2021Article
- Ca2+ administration prevents α-synuclein proteotoxicity by stimulating calcineurin-dependent lysosomal proteolysis.PLoS genetics · 2021Article
- Endonuclease G promotes autophagy by suppressing mTOR signaling and activating the DNA damage response.Nature communications · 2021Article
- Modeling Parkinson's Disease: Not Only Rodents?Frontiers in aging neuroscience · 2021Article
Corrections and comments
- Commented on by
Authors and funding
29 authors at 8 institutions in 5 countries.
Funding
Abstract
Malfunctioning of the protein α-synuclein is critically involved in the demise of dopaminergic neurons relevant to Parkinson's disease. Nonetheless, the precise mechanisms explaining this pathogenic neuronal cell death remain elusive. Endonuclease G (EndoG) is a mitochondrially localized nuclease that triggers DNA degradation and cell death upon translocation from mitochondria to the nucleus. Here, we show that EndoG displays cytotoxic nuclear localization in dopaminergic neurons of human Parkinson-diseased patients, while EndoG depletion largely reduces α-synuclein-induced cell death in human neuroblastoma cells. Xenogenic expression of human α-synuclein in yeast cells triggers mitochondria-nuclear translocation of EndoG and EndoG-mediated DNA degradation through a mechanism that requires a functional kynurenine pathway and the permeability transition pore. In nematodes and flies, EndoG is essential for the α-synuclein-driven degeneration of dopaminergic neurons. Moreover, the locomotion and survival of α-synuclein-expressing flies is compromised, but reinstalled by parallel depletion of EndoG. In sum, we unravel a phylogenetically conserved pathway that involves EndoG as a critical downstream executor of α-synuclein cytotoxicity.
Indexed as
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.