Evidence map›Paper›PMID 25905039›Full record

ReviewFrontiers in oncology2015

The eEF1A Proteins: At the Crossroads of Oncogenesis, Apoptosis, and Viral Infections.

Wasim Abbas, Amit Kumar, Georges Herbein

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers.

0numbers the graph read from it
0cells of the map it votes in
129citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

129 citing papers in PubMed, 212 citations in OpenAlex.

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  13. BE-43547AActa pharmacologica Sinica · 2025
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69 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 2 countries.

Wasim AbbasDepartment of Biology, SBA School of Science and Engineering, Lahore University of Management Sciences , Lahore , Pakistan.
Amit KumarUPRES EA 4266, Laboratory of Pathogens and Inflammation, Department of Virology, CHRU Besançon, Université de Franche-Comté , Besançon , France.
Georges HerbeinUPRES EA 4266, Laboratory of Pathogens and Inflammation, Department of Virology, CHRU Besançon, Université de Franche-Comté , Besançon , France.
Université de franche-comté · FRLahore University of Management Sciences · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Eukaryotic translation elongation factors 1 alpha, eEF1A1 and eEF1A2, are not only translation factors but also pleiotropic proteins that are highly expressed in human tumors, including breast cancer, ovarian cancer, and lung cancer. eEF1A1 modulates cytoskeleton, exhibits chaperone-like activity and also controls cell proliferation and cell death. In contrast, eEF1A2 protein favors oncogenesis as shown by the fact that overexpression of eEF1A2 leads to cellular transformation and gives rise to tumors in nude mice. The eEF1A2 protein stimulates the phospholipid signaling and activates the Akt-dependent cell migration and actin remodeling that ultimately favors tumorigenesis. In contrast, inactivation of eEF1A proteins leads to immunodeficiency, neural and muscular defects, and favors apoptosis. Finally, eEF1A proteins interact with several viral proteins resulting in enhanced viral replication, decreased apoptosis, and increased cellular transformation. This review summarizes the recent findings on eEF1A proteins indicating that eEF1A proteins play a critical role in numerous human diseases through enhancement of oncogenesis, blockade of apoptosis, and increased viral pathogenesis.

Indexed as

apoptosiscancereEF1AHIVvirus

Identifiers

PMID25905039
PMCPMC4387925
OpenAlexW1995316524

What OpenQuestion holds

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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.