ArticleCells2022
Systematic Functional Analysis of
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 22 citations in OpenAlex.
- miRNA family miR-29 inhibits PINK1-PRKN signaling via ATG9A.Molecular neurodegeneration advances · 2026Article
- Autophagy and mitophagy at the synapse and beyond: implications for learning, memory and neurological disorders.Autophagy · 2026Review
- Novel insight into PINK1/parkin-associated autophagy implicated in Parkinson disease.Translational neuroscience · 2026Review
- Activation of endogenous PRKN by structural derepression is linked to increased turnover of the E3 ubiquitin ligase.Autophagy · 2025Article
- Review
- Inborn errors of canonical autophagy in neurodegenerative diseases.Human molecular genetics · 2025Review
- Gut Permeability and Microbiota in Parkinson's Disease: Mechanistic Insights and Experimental Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Article
- Genomic and Transcriptomic Approaches Advance the Diagnosis and Prognosis of Neurodegenerative Diseases.Genes · 2025Review
- Protein quality control systems in neurodegeneration - culprits, mitigators, and solutions?Frontiers in neurology · 2025Review
- Ubiquitin system mutations in neurological diseases.Trends in biochemical sciences · 2024Review
- Activation of parkin by a molecular glue.Nature communications · 2024Article
- Structural and Functional Characterization of the Most Frequent Pathogenic PRKN Substitution p.R275W.Cells · 2024Article
- Naturally occurring hyperactive variants of human parkin.Communications biology · 2024Article
- Article
- A Functional Schizophrenia-associated genetic variant near thebioRxiv : the preprint server for biology · 2023Article
- Herpes Simplex Virus Type 1 Induces AD-like Neurodegeneration Markers in Human Progenitor and Differentiated ReNcell VM Cells.Microorganisms · 2023Article
- Proximity-labeling chemoproteomics defines the subcellular cysteinome and inflammation-responsive mitochondrial redoxome.bioRxiv : the preprint server for biology · 2023Article
- Review
- Post-translational modification and mitochondrial function in Parkinson's disease.Frontiers in molecular neuroscience · 2023Review
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 1 institution in 1 country.
Funding
Abstract
Loss of either PINK1 or PRKN causes an early onset Parkinson's disease (PD) phenotype. Functionally, PINK1 and PRKN work together to mediate stress-activated mitochondrial quality control. Upon mitochondrial damage, PINK1, a ubiquitin kinase and PRKN, a ubiquitin ligase, decorate damaged organelles with phosphorylated ubiquitin for sequestration and degradation in lysosomes, a process known as mitophagy. While several genetic mutations are established to result in loss of mitophagy function, many others have not been extensively characterized and are of unknown significance. Here, we analyzed a set of twenty variants, ten in each gene, focusing on understudied variants mostly from the Parkinson's progressive marker initiative, with sensitive assays to define potential functional deficits. Our results nominate specific rare genetic
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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.