Evidence map›Paper›PMID 24244333›Full record

ArticlePloS one2013

Profiling of Parkin-binding partners using tandem affinity purification.

Alessandra Zanon, Aleksandar Rakovic, Hagen Blankenburg, Nadezhda T Doncheva, Christine Schwienbacher, Alice Serafin, Adrian Alexa, Christian X Weichenberger, Mario Albrecht, Christine Klein and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.7field-weighted citation impact, top 5% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Genetic Sketch of Parkinson's Disease in India.Annals of Indian Academy of Neurology · 2025
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  7. Molecular Mechanisms for Changing Brain Connectivity in Mice and Humans.International journal of molecular sciences · 2023
    Article
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  9. Fluorescent reporter ofOpen research Europe · 2022
    Article
  10. Predictors of prodromal Parkinson's disease in young adultFrontiers in behavioral neuroscience · 2022
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 2 countries.

Alessandra ZanonCenter for Biomedicine, European Academy Bozen/Bolzano (EURAC), Bolzano, Italy, Affiliated Institute of the University of Lübeck, Lübeck, Germany.
Aleksandar Rakovic
Hagen Blankenburg
Nadezhda T Doncheva
Christine Schwienbacher
Alice Serafin
Adrian Alexa
Christian X Weichenberger
Mario Albrecht
Christine Klein
Andrew A Hicks
Peter P Pramstaller
Francisco S Domingues
Irene Pichler
Eurac Research · ITBecker Technologies (Germany) · DEMax Planck Institute for Informatics · DEUniversitätsmedizin Greifswald · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disorder affecting approximately 1-2% of the general population over age 60. It is characterized by a rather selective loss of dopaminergic neurons in the substantia nigra and the presence of α-synuclein-enriched Lewy body inclusions. Mutations in the Parkin gene (PARK2) are the major cause of autosomal recessive early-onset parkinsonism. The Parkin protein is an E3 ubiquitin ligase with various cellular functions, including the induction of mitophagy upon mitochondrial depolarizaton, but the full repertoire of Parkin-binding proteins remains poorly defined. Here we employed tandem affinity purification interaction screens with subsequent mass spectrometry to profile binding partners of Parkin. Using this approach for two different cell types (HEK293T and SH-SY5Y neuronal cells), we identified a total of 203 candidate Parkin-binding proteins. For the candidate proteins and the proteins known to cause heritable forms of parkinsonism, protein-protein interaction data were derived from public databases, and the associated biological processes and pathways were analyzed and compared. Functional similarity between the candidates and the proteins involved in monogenic parkinsonism was investigated, and additional confirmatory evidence was obtained using published genetic interaction data from Drosophila melanogaster. Based on the results of the different analyses, a prioritization score was assigned to each candidate Parkin-binding protein. Two of the top ranking candidates were tested by co-immunoprecipitation, and interaction to Parkin was confirmed for one of them. New candidates for involvement in cell death processes, protein folding, the fission/fusion machinery, and the mitophagy pathway were identified, which provide a resource for further elucidating Parkin function.

Indexed as

AnimalsCell Line, TumorDrosophila melanogasterDrosophila ProteinsHumansNerve Tissue ProteinsParkinson DiseaseProtein BindingUbiquitin-Protein LigasesDrosophila ProteinsNerve Tissue Proteinsparkin proteinpark protein, DrosophilaUbiquitin-Protein Ligases

Identifiers

PMID24244333
PMCPMC3823883
OpenAlexW2039586060

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

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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.