ReviewMolecular medicine reports2025
Spliceosome protein EFTUD2: A potential pathogenetic factor in tumorigenesis and some developmental defects (Review).
Review in Molecular medicine reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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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.
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Who cites it
4 citing papers in PubMed.
- Network Clustering Approach Reveals Key Proteins and Biological Functions in the Response of Whiteleg Shrimp (Penaeus vannamei) to Acute Hepatopancreatic Necrosis Disease.Marine biotechnology (New York, N.Y.) · 2026Article
- S-Doped Carbon Dot Treatment Alters RNA Processing, Translation, and Protein Degradation Pathways in HeLa Cells.Current issues in molecular biology · 2026Article
- Recurrent mandibulofacial dysostosis, Guion-Almeida type in consecutive pregnancies due to maternal mosaicism of a novel EFTUD2 variant: a case report and review of the literature.Journal of medical case reports · 2026Review
- A novelTranslational pediatrics · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The formation of mature mRNA is inseparable from the processing of RNA precursors and splicing by the spliceosome. The spliceosome is a multi‑protein complex composed of five small nuclear ribonucleoproteins. Elongation factor Tu GTP binding domain containing 2 (EFTUD2) is a component of spliceosome complex that is involved in the reorganization of the spliceosome complex, thereby promoting the removal of introns from precursor mRNA. Therefore, EFTUD2 can regulate embryonic development and innate immunity by modulating the splicing of various mRNAs. The mutations in EFTUD2 itself also lead to developmental defects and clinical manifestations in mandibulofacial dysostosis, the nervous system, the circulatory system, the digestive system and the reproductive system. Furthermore, the overexpression of EFTUD2 promotes the progression of hepatocellular carcinoma, breast cancer and colorectal cancer. The present review discussed the molecular mechanisms by which EFTUD2 exerts its physiological functions, focusing on EFTUD2 mutations and their corresponding clinical manifestations. It aimed to provide insight for the diagnosis and treatment of EFTUD2‑related diseases.
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Registered trials
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