Evidence map›Paper›PMID 36123349›Full record

ArticleCell death discovery2022

Overexpressing eukaryotic elongation factor 1 alpha (eEF1A) proteins to promote corticospinal axon repair after injury.

Daniel Romaus-Sanjurjo, Junmi M Saikia, Hugo J Kim, Kristen M Tsai, Geneva Q Le, Binhai Zheng

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

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  10. Roles of Kdm6a and Kdm6b in Regulation of Mammalian Neural Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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  15. Genome-wide analysis of the soybeanFrontiers in plant science · 2024
    Article
  16. Article
  17. Autism- and epilepsy-associatedProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  18. Article
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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

6 authors at 2 institutions in 2 countries.

Daniel Romaus-SanjurjoDepartment of Neurosciences, School of Medicine, University of California San Diego, La Jolla, CA, 92093, USA.
Junmi M SaikiaDepartment of Neurosciences, School of Medicine, University of California San Diego, La Jolla, CA, 92093, USA.
Hugo J KimDepartment of Neurosciences, School of Medicine, University of California San Diego, La Jolla, CA, 92093, USA.ORCID http://orcid.org/0000-0002-8610-9677
Kristen M TsaiDepartment of Neurosciences, School of Medicine, University of California San Diego, La Jolla, CA, 92093, USA.ORCID http://orcid.org/0000-0003-2336-2672
Geneva Q LeDepartment of Neurosciences, School of Medicine, University of California San Diego, La Jolla, CA, 92093, USA.
Binhai ZhengDepartment of Neurosciences, School of Medicine, University of California San Diego, La Jolla, CA, 92093, USA. bizheng@health.ucsd.edu.ORCID http://orcid.org/0000-0003-3906-3722
University of California San Diego · USUC San Diego Health System · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007198 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHI, NEIL C, INSEL, PAUL A · 1985 to 2024
$29.3M
Viral ModuleP30EY012196 · NEI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI ZHIGANG HE · 1998 to 2026
$21.3M
U of Calif, San Diego Neuroscience Microscopy ImagingP30NS047101 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLEESON, JOSEPH G, ZHENG, BINHAI · 2003 to 2022
$9.0M
The Role of a Pair of MAP3Ks in the Multicellular Response to Spinal Cord InjuryR01NS093055 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ZHENG, BINHAI · 2015 to 2024
$4.0M
Genetic analysis of myelin inhibitors and PTEN in injury-inducedCNS axon growthR01NS054734 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ZHENG, BINHAI · 2007 to 2015
$3.2M
Harnessing Corticospinal Axon Sprouting for Functional Recovery in Chronic InjuryI01RX002483 · VA · VA SAN DIEGO HEALTHCARE SYSTEM · PI ZHENG, BINHAI · 2019 to 2023
–
Craig H. Neilsen Foundation (Neilsen Foundation) 384971Craig H. Neilsen Foundation (Neilsen Foundation) 648861Craig H. Neilsen Foundation (Neilsen Foundation) 733544NEI NIH HHS P30 EY012196NIGMS NIH HHS T32 GM007198NINDS NIH HHS P30 NS047101NINDS NIH HHS R01 NS054734NINDS NIH HHS R01 NS093055RRD VA I01 RX002483U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS) NS047101U.S. Department of Veterans Affairs (Department of Veterans Affairs) RX002483Wings for Life (Wings for Life Research Foundation) WFL-US-27/17
6 · The paper itself

Abstract

Although protein synthesis is hypothesized to have a pivotal role in axonal repair after central nervous system (CNS) injury, the role of core components of the protein synthesis machinery has not been examined. Notably, some elongation factors possess non-canonical functions that may further impact axonal repair. Here, we examined whether overexpressing eukaryotic elongation factor 1 alpha (eEF1A) proteins enhances the collateral sprouting of corticospinal tract (CST) neurons after unilateral pyramidotomy, along with the underlying molecular mechanisms. We found that overexpressing eEF1A proteins in CST neurons increased the levels of pS6, an indicator for mTOR activity, but not pSTAT3 and pAKT levels, in neuronal somas. Strikingly, overexpressing eEF1A2 alone, but neither eEF1A1 alone nor both factors simultaneously, increased protein synthesis and actin rearrangement in CST neurons. While eEF1A1 overexpression only slightly enhanced CST sprouting after pyramidotomy, eEF1A2 overexpression substantially enhanced this sprouting. Surprisingly, co-overexpression of both eEF1A1 and eEF1A2 led to a sprouting phenotype similar to wild-type controls, suggesting an antagonistic effect of overexpressing both proteins. These data provide the first evidence that overexpressing a core component of the translation machinery, eEF1A2, enhances CST sprouting, likely by a combination of increased protein synthesis, mTOR signaling and actin cytoskeleton rearrangement.

Identifiers

PMID36123349
PMCPMC9485247
OpenAlexW4296460187

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.