Evidence map›Paper›PMID 32088381›Full record

ArticleNeurobiology of disease2020

DYNLRB1 is essential for dynein mediated transport and neuronal survival.

Marco Terenzio, Agostina Di Pizio, Ida Rishal, Letizia Marvaldi, Pierluigi Di Matteo, Riki Kawaguchi, Giovanni Coppola, Giampietro Schiavo, Elizabeth M C Fisher, Mike Fainzilber

Open access · goldAbstract read
In one paragraph

Article in Neurobiology of disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

20 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. A mutation inMolecular vision · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. The Green Valley ofCells · 2022
    Review
  18. Article
  19. Article
  20. Article
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

10 authors at 5 institutions in 4 countries.

Marco TerenzioDepartment of Biomolecular Sciences, Weizmann Institute of Science, Rehovot 7610001, Israel; Molecular Neuroscience Unit, Okinawa Institute of Science and Technology Graduate University, Kunigami-gun, Okinawa 904-0412, Japan. Electronic address: marco.terenzio@oist.jp.
Agostina Di PizioDepartment of Biomolecular Sciences, Weizmann Institute of Science, Rehovot 7610001, Israel.
Ida RishalDepartment of Biomolecular Sciences, Weizmann Institute of Science, Rehovot 7610001, Israel.
Letizia MarvaldiDepartment of Biomolecular Sciences, Weizmann Institute of Science, Rehovot 7610001, Israel.
Pierluigi Di MatteoDepartment of Biomolecular Sciences, Weizmann Institute of Science, Rehovot 7610001, Israel.
Riki KawaguchiDepartments of Psychiatry and Neurology, Semel Institute for Neuroscience and Human Behavior, University of California Los Angeles, Los Angeles, CA 90095, USA.
Giovanni CoppolaDepartments of Psychiatry and Neurology, Semel Institute for Neuroscience and Human Behavior, University of California Los Angeles, Los Angeles, CA 90095, USA.
Giampietro SchiavoDepartment of Neuromuscular Diseases, UCL Queen Square Institute of Neurology, Queen Square, London WC1N 3BG, UK; UK Dementia Research Institute, University College London, London WC1E 6BT, UK; Discoveries Centre for Regenerative and Precision Medicine, University College London Campus, London WC1N 3BG, UK.
Elizabeth M C FisherDepartment of Neuromuscular Diseases, UCL Queen Square Institute of Neurology, Queen Square, London WC1N 3BG, UK.
Mike FainzilberDepartment of Biomolecular Sciences, Weizmann Institute of Science, Rehovot 7610001, Israel.
Weizmann Institute of Science · ILUniversity of California, Los Angeles · USNational Hospital for Neurology and Neurosurgery · GBOkinawa Institute of Science and Technology Graduate University · JPUK Dementia Research Institute · GB

Funding

Medical Research Council G0500288Wellcome Trust 107116/Z/15/Z
6 · The paper itself

Abstract

The cytoplasmic dynein motor complex transports essential signals and organelles from the cell periphery to the perinuclear region, hence is critical for the survival and function of highly polarized cells such as neurons. Dynein Light Chain Roadblock-Type 1 (DYNLRB1) is thought to be an accessory subunit required for specific cargos, but here we show that it is essential for general dynein-mediated transport and sensory neuron survival. Homozygous Dynlrb1 null mice are not viable and die during early embryonic development. Furthermore, heterozygous or adult knockdown animals display reduced neuronal growth, and selective depletion of Dynlrb1 in proprioceptive neurons compromises their survival. Conditional depletion of Dynlrb1 in sensory neurons causes deficits in several signaling pathways, including β-catenin subcellular localization, and a severe impairment in the axonal transport of both lysosomes and retrograde signaling endosomes. Hence, DYNLRB1 is an essential component of the dynein complex, and given dynein's critical functions in neuronal physiology, DYNLRB1 could have a prominent role in the etiology of human neurodegenerative diseases.

Indexed as

AnimalsAxonal TransportCarrier ProteinsCells, CulturedCell SurvivalDyneinsLysosomesMaleMiceNeurogenesisOrganellesSensory Receptor CellsTransfectionCarrier ProteinsDyneinsAxonal transportDynein complexdynlrb1NeurodegenerationNeuronal survival

Identifiers

PMID32088381
PMCPMC7273200
OpenAlexW3007208575

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.