Evidence map›Paper›PMID 25316086›Full record

ArticleNature communications2014

Parkin regulates kainate receptors by interacting with the GluK2 subunit.

AnnaMaria Maraschi, Andrea Ciammola, Alessandra Folci, Francesca Sassone, Giuseppe Ronzitti, Graziella Cappelletti, Vincenzo Silani, Shigeto Sato, Nobutaka Hattori, Michele Mazzanti and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.1field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Roles of Glutamate Receptors in Parkinson's Disease.International journal of molecular sciences · 2019
    Review
  18. Are we listening to everything the PARK genes are telling us?The Journal of comparative neurology · 2019
    Review
  19. Review
  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 6 institutions in 3 countries.

AnnaMaria MaraschiIRCCS Istituto Auxologico Italiano, Department of Neurology and Laboratory of Neuroscience, Cusano Milanino, 20095 Milan, Italy.
Andrea CiammolaIRCCS Istituto Auxologico Italiano, Department of Neurology and Laboratory of Neuroscience, Cusano Milanino, 20095 Milan, Italy.
Alessandra FolciCNR Institute of Neuroscience, Department of BIOMETRA, University of Milan, 20129 Milan, Italy.
Francesca SassoneIRCCS Istituto Auxologico Italiano, Department of Neurology and Laboratory of Neuroscience, Cusano Milanino, 20095 Milan, Italy.
Giuseppe RonzittiDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, 16163 Genova, Italy.
Graziella CappellettiDepartment of Biosciences, Università degli Studi di Milano, 20122 Milan, Italy.
Vincenzo Silani1] IRCCS Istituto Auxologico Italiano, Department of Neurology and Laboratory of Neuroscience, Cusano Milanino, 20095 Milan, Italy [2] 'Dino Ferrari' Center, Department of Pathophysiology and Transplantation, Università degli Studi di Milano, 20122 Milan, Italy.
Shigeto SatoDepartment of Neurology, Juntendo University School of Medicine, 113-8421 Tokyo, Japan.
Nobutaka HattoriDepartment of Neurology, Juntendo University School of Medicine, 113-8421 Tokyo, Japan.
Michele MazzantiDepartment of Biosciences, Università degli Studi di Milano, 20122 Milan, Italy.
Evelina ChieregattiDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, 16163 Genova, Italy.
Christophe MulleInterdisciplinary Institute for Neuroscience, CNRS UMR 5297, University of Bordeaux, 33000 Bordeaux, France.
Maria PassafaroCNR Institute of Neuroscience, Department of BIOMETRA, University of Milan, 20129 Milan, Italy.
Jenny SassoneIRCCS Istituto Auxologico Italiano, Department of Neurology and Laboratory of Neuroscience, Cusano Milanino, 20095 Milan, Italy.
IRCCS Istituto Auxologico Italiano · ITUniversity of Milan · ITItalian Institute of Technology · ITJuntendo University · JPIstituti di Ricovero e Cura a Carattere Scientifico · ITUniversité de Bordeaux · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although loss-of-function mutations in the PARK2 gene, the gene that encodes the protein parkin, cause autosomal recessive juvenile parkinsonism, the responsible molecular mechanisms remain unclear. Evidence suggests that a loss of parkin dysregulates excitatory synapses. Here we show that parkin interacts with the kainate receptor (KAR) GluK2 subunit and regulates KAR function. Loss of parkin function in primary cultured neurons causes GluK2 protein to accumulate in the plasma membrane, potentiates KAR currents and increases KAR-dependent excitotoxicity. Expression in the mouse brain of a parkin mutant causing autosomal recessive juvenile parkinsonism results in GluK2 protein accumulation and excitotoxicity. These findings show that parkin regulates KAR function in vitro and in vivo, and suggest that KAR upregulation may have a pathogenetic role in parkin-related autosomal recessive juvenile parkinsonism.

Indexed as

AnimalsCell MembraneDisease Models, AnimalFemaleGluK2 Kainate ReceptorHumansKainic Acid ReceptorsMiceMice, TransgenicNeuronsParkinsonian DisordersProtein BindingRatsUbiquitin-Protein LigasesGluK2 Kainate ReceptorKainic Acid Receptorsparkin proteinUbiquitin-Protein Ligases

Identifiers

PMID25316086
PMCPMC4218952
OpenAlexW1974175558

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.