Evidence map›Paper›PMID 38219147›Full record

ArticleCell reports2024

The integrated stress response effector GADD34 is repurposed by neurons to promote stimulus-induced translation.

Mauricio M Oliveira, Muhaned Mohamed, Megan K Elder, Keylin Banegas-Morales, Maggie Mamcarz, Emily H Lu, Ela A N Golhan, Nishika Navrange, Snehajyoti Chatterjee, Ted Abel and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Distinct cell type-specific mechanisms underlie cognitive dysfunction during persistent integrated stress response activation.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

11 authors at 2 institutions in 1 country.

Mauricio M OliveiraCenter for Neural Science, New York University, New York, NY, USA.
Muhaned MohamedCenter for Neural Science, New York University, New York, NY, USA.
Megan K ElderCenter for Neural Science, New York University, New York, NY, USA.
Keylin Banegas-MoralesCenter for Neural Science, New York University, New York, NY, USA.
Maggie MamcarzCenter for Neural Science, New York University, New York, NY, USA.
Emily H LuCenter for Neural Science, New York University, New York, NY, USA.
Ela A N GolhanCenter for Neural Science, New York University, New York, NY, USA.
Nishika NavrangeCenter for Neural Science, New York University, New York, NY, USA.
Snehajyoti ChatterjeeDepartment of Neuroscience and Pharmacology, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
Ted AbelDepartment of Neuroscience and Pharmacology, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
Eric KlannCenter for Neural Science, New York University, New York, NY, USA; NYU Neuroscience Institute, New York University School of Medicine, New York, NY, USA. Electronic address: ek65@nyu.edu.
New York University · USUniversity of Iowa · US

Funding

Pulmonary Toxicology Facility CoreP30ES005605 · NIEHS · UNIVERSITY OF IOWA · PI Jong Sung Kim · 1990 to 2026
$40.5M
Translational Control in Memory and Brain DisordersR35NS122316 · NINDS · NEW YORK UNIVERSITY · PI Eric Klann · 2021 to 2026
$6.5M
eIF2alpha Phosphorylation in Synaptic Plasticity, Memory, and Brain DisordersR37NS034007 · NINDS · NEW YORK UNIVERSITY · PI KLANN, ERIC · 2014 to 2020
$3.3M
Dysregulated Ribosomal Protein Synthesis in Amyloid and Tau Mouse ModelsR21NS121786 · NINDS · NEW YORK UNIVERSITY · PI KLANN, ERIC · 2021 to 2021
$436k
NIEHS NIH HHS P30 ES005605NINDS NIH HHS R21 NS121786NINDS NIH HHS R35 NS122316NINDS NIH HHS R37 NS034007
6 · The paper itself

Abstract

Neuronal protein synthesis is required for long-lasting plasticity and long-term memory consolidation. Dephosphorylation of eukaryotic initiation factor 2α is one of the key translational control events that is required to increase de novo protein synthesis that underlies long-lasting plasticity and memory consolidation. Here, we interrogate the molecular pathways of translational control that are triggered by neuronal stimulation with brain-derived neurotrophic factor (BDNF), which results in eukaryotic initiation factor 2α (eIF2α) dephosphorylation and increases in de novo protein synthesis. Primary rodent neurons exposed to BDNF display elevated translation of GADD34, which facilitates eIF2α dephosphorylation and subsequent de novo protein synthesis. Furthermore, GADD34 requires G-actin generated by cofilin to dephosphorylate eIF2α and enhance protein synthesis. Finally, GADD34 is required for BDNF-induced translation of synaptic plasticity-related proteins. Overall, we provide evidence that neurons repurpose GADD34, an effector of the integrated stress response, as an orchestrator of rapid increases in eIF2-dependent translation in response to plasticity-inducing stimuli.

Indexed as

Actin Depolymerizing FactorsBrain-Derived Neurotrophic FactorActinsEukaryotic Initiation Factor-2NeuronsActin Depolymerizing FactorsActinsBrain-Derived Neurotrophic FactorEukaryotic Initiation Factor-2BDNFCP: Molecular biologyCP: NeurosciencecytoskeletoneIF2αGADD34local translationmRNA translationneuronneuronal plasticityprotein synthesissynaptic plasticity

Identifiers

PMID38219147
PMCPMC10964249
OpenAlexW4390848265

What Socratic 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 Socratic graph.