Evidence map›Paper›PMID 29084947›Full record

ArticleNature communications2017

Plekhg5-regulated autophagy of synaptic vesicles reveals a pathogenic mechanism in motoneuron disease.

Patrick Lüningschrör, Beyenech Binotti, Benjamin Dombert, Peter Heimann, Angel Perez-Lara, Carsten Slotta, Nadine Thau-Habermann, Cora R von Collenberg, Franziska Karl, Markus Damme and 12 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Guideline
  2. Synaptic Proteostasis in Health and Disease.Journal of neurochemistry · 2026
    Review
  3. Junctions in Jeopardy: the neuromuscular junction is a selective pathological target in Charcot-Marie-Tooth disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Turning garbage into gold: Autophagy in synaptic function.Current opinion in neurobiology · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Epigenetic regulation ofAutophagy · 2024
    Review
  15. NeuronalCells · 2023
    Article
  16. Review
  17. Article
  18. Review
  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

22 authors at 8 institutions in 4 countries.

Patrick LüningschrörInstitute of Clinical Neurobiology, University Hospital Würzburg, 97078, Würzburg, Germany.
Beyenech BinottiDepartment of Neurobiology, Max Planck Institute for Biophysical Chemistry, 37077, Göttingen, Germany.
Benjamin DombertInstitute of Clinical Neurobiology, University Hospital Würzburg, 97078, Würzburg, Germany.
Peter HeimannDepartment of Cell Biology, University of Bielefeld, 33501, Bielefeld, Germany.
Angel Perez-LaraDepartment of Neurobiology, Max Planck Institute for Biophysical Chemistry, 37077, Göttingen, Germany.ORCID http://orcid.org/0000-0002-2736-3501
Carsten SlottaDepartment of Cell Biology, University of Bielefeld, 33501, Bielefeld, Germany.
Nadine Thau-HabermannDepartment of Neurology, Hannover Medical School, 30625, Hannover, Germany.
Cora R von CollenbergInstitute of Clinical Neurobiology, University Hospital Würzburg, 97078, Würzburg, Germany.
Franziska KarlDepartment of Neurology, University Hospital Würzburg, 97078, Würzburg, Germany.
Markus DammeInstitut für Biochemie, Christian-Albrechts-Universität zu Kiel, 24098, Kiel, Germany.
Arie HorowitzCardeza Vascular Biology Center, Departments of Medicine and Cancer Biology, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA, 19107, USA.ORCID http://orcid.org/0000-0001-6239-1287
Isabelle MaystadtCentre de Génétique Humaine, Institut de Pathologie et de Génétique, 6041, Gosselies, Belgium.
Annette FüchtbauerDepartment of Molecular Biology and Genetics, Aarhus University, 8000, Aarhus C, Denmark.
Ernst-Martin FüchtbauerDepartment of Molecular Biology and Genetics, Aarhus University, 8000, Aarhus C, Denmark.
Sibylle JablonkaInstitute of Clinical Neurobiology, University Hospital Würzburg, 97078, Würzburg, Germany.
Robert BlumInstitute of Clinical Neurobiology, University Hospital Würzburg, 97078, Würzburg, Germany.
Nurcan ÜçeylerDepartment of Neurology, University Hospital Würzburg, 97078, Würzburg, Germany.
Susanne PetriDepartment of Neurology, Hannover Medical School, 30625, Hannover, Germany.
Barbara KaltschmidtDepartment of Cell Biology, University of Bielefeld, 33501, Bielefeld, Germany.
Reinhard JahnDepartment of Neurobiology, Max Planck Institute for Biophysical Chemistry, 37077, Göttingen, Germany.
Christian KaltschmidtDepartment of Cell Biology, University of Bielefeld, 33501, Bielefeld, Germany. c.kaltschmidt@uni-bielefeld.de.
Michael SendtnerInstitute of Clinical Neurobiology, University Hospital Würzburg, 97078, Würzburg, Germany. Sendtner_M@ukw.de.ORCID http://orcid.org/0000-0002-4737-2974
Universitätsklinikum Würzburg · DEBielefeld University · DEMax Planck Institute for Biophysical Chemistry · DEAarhus University · DKMedizinische Hochschule Hannover · DEChristian-Albrechts-Universität zu Kiel · DEInstitute of Pathology and Genetics · BEThomas Jefferson University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy-mediated degradation of synaptic components maintains synaptic homeostasis but also constitutes a mechanism of neurodegeneration. It is unclear how autophagy of synaptic vesicles and components of presynaptic active zones is regulated. Here, we show that Pleckstrin homology containing family member 5 (Plekhg5) modulates autophagy of synaptic vesicles in axon terminals of motoneurons via its function as a guanine exchange factor for Rab26, a small GTPase that specifically directs synaptic vesicles to preautophagosomal structures. Plekhg5 gene inactivation in mice results in a late-onset motoneuron disease, characterized by degeneration of axon terminals. Plekhg5-depleted cultured motoneurons show defective axon growth and impaired autophagy of synaptic vesicles, which can be rescued by constitutively active Rab26. These findings define a mechanism for regulating autophagy in neurons that specifically targets synaptic vesicles. Disruption of this mechanism may contribute to the pathophysiology of several forms of motoneuron disease.

Indexed as

AnimalsAutophagyCell LineCells, CulturedGuanine Nucleotide Exchange FactorsMice, Inbred C57BLMice, KnockoutMice, TransgenicMicroscopy, Electron, TransmissionMotor Neuron DiseaseMotor NeuronsPresynaptic Terminalsrab GTP-Binding ProteinsSynaptic VesiclesGuanine Nucleotide Exchange FactorsRab26 protein, mouserab GTP-Binding ProteinsSyx protein, mouse

Identifiers

PMID29084947
PMCPMC5662736
OpenAlexW2756273498

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.