Evidence map›Paper›PMID 33046555›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2020

4E-BP1 Protects Neurons from Misfolded Protein Stress and Parkinson's Disease Toxicity by Inducing the Mitochondrial Unfolded Protein Response.

Somasish Ghosh Dastidar, Michael T Pham, Matthew B Mitchell, Steven G Yeom, Sarah Jordan, Angela Chang, Bryce L Sopher, Albert R La Spada

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 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
1.3field-weighted citation impact, top 16% 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, 25 citations in OpenAlex.

  1. Review
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  7. Identification of Key Active Constituents inInternational journal of molecular sciences · 2025
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  16. SIGMAR1 Confers Innate Resilience against Neurodegeneration.International journal of molecular sciences · 2023
    Review
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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

8 authors at 5 institutions in 2 countries.

Somasish Ghosh DastidarDepartments of Neurology, Neurobiology, and Cell Biology, Duke University School of Medicine, Durham, North Carolina 27710 alaspada@uci.edu somasish.gd@manipal.edu.
Michael T PhamDepartments of Neurology, Neurobiology, and Cell Biology, Duke University School of Medicine, Durham, North Carolina 27710.
Matthew B MitchellDepartment of Pediatrics, and the Institute for Genomic Medicine, University of California, San Diego, California 92093.
Steven G YeomDepartment of Pediatrics, and the Institute for Genomic Medicine, University of California, San Diego, California 92093.
Sarah JordanDepartment of Pediatrics, and the Institute for Genomic Medicine, University of California, San Diego, California 92093.
Angela ChangDepartment of Pediatrics, and the Institute for Genomic Medicine, University of California, San Diego, California 92093.
Bryce L SopherDepartment of Neurology, University of Washington Medical Center, Seattle, Washington 98195.
Albert R La SpadaDepartments of Neurology, Neurobiology, and Cell Biology, Duke University School of Medicine, Durham, North Carolina 27710 alaspada@uci.edu somasish.gd@manipal.edu.
University of California, San Diego · USDuke University · USKasturba Medical College, Manipal · INUniversity of California, Irvine · USUniversity of Washington Medical Center · US

Funding

The PPAR-delta pathway in neural function and Huntington's disease neuropathologyR01NS065874 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LA SPADA, ALBERT R · 2010 to 2020
$4.0M
Molecular genetic regulation of autophagy in health and neurodegenerative diseaseR01AG033082 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LA SPADA, ALBERT R · 2009 to 2019
$4.0M
NIA NIH HHS R01 AG033082NINDS NIH HHS R01 NS065874
6 · The paper itself

Abstract

Decline of protein quality control in neurons contributes to age-related neurodegenerative disorders caused by misfolded proteins. 4E-BP1 is a key node in the regulation of protein synthesis, as activated 4E-BP1 represses global protein translation. Overexpression of 4E-BP1 mediates the benefits of dietary restriction and can counter metabolic stress, and 4E-BP1 disinhibition on mTORC1 repression may be neuroprotective; however, whether 4E-BP1 overexpression is neuroprotective in mammalian neurons is yet to be fully explored. To address this question, we generated 4E-BP1-overexpressing transgenic mice and confirmed marked reductions in protein translation in 4E-BP1-overexpressing primary neurons. After documenting that 4E-BP1-overexpressing neurons are resistant to proteotoxic stress elicited by brefeldin A treatment, we exposed primary neurons to three different Parkinson's disease (PD)-linked toxins (rotenone, maneb, or paraquat) and documented significant protection in neurons from newborn male and female

Indexed as

Protein UnfoldingAdaptor Proteins, Signal Transducingalpha-SynucleinAnimalsAnimals, NewbornBrefeldin ACell Cycle ProteinsFemaleMaleMiceMice, TransgenicMitochondriaNeuronsParkinson Disease, SecondaryPrimary Cell CultureProtein BiosynthesisAdaptor Proteins, Signal Transducingalpha-SynucleinBrefeldin ACell Cycle ProteinsEif4ebp1 protein, mouseProtein Synthesis InhibitorsRotenoneUncoupling Agents4E-BP1alpha-synucleinmitochondrial unfolded protein responseneuroprotectionParkinson's diseaseprotein translation

Identifiers

PMID33046555
PMCPMC7643294
OpenAlexW3092068410

What OpenQuestion holds

Textmetadata
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.