1997/02/01 by Shinya Yamanaka, Karen S. Poksay, K S Arnold +1 · 3 citations
Biochemistry, Genetics and Molecular Biology · #RNA and protein synthesis mechanisms #RNA regulation and disease #RNA Research and Splicing
paper · pdf · doi:10.1101/gad.11.3.321
openalex publication_date 1997/02/01 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/01
Transgene expression of the apolipoprotein B mRNA-editing enzyme (APOBEC-1) causes dysplasia and carcinoma in mouse and rabbit livers. Using a modified differential display technique, we identified a novel mRNA (NAT1 for novel APOBEC-1 target no. 1) that is extensively edited at multiple sites in these livers. The aberrant editing alters encoded amino acids, creates stop codons, and results in markedly reduced levels of the NAT1 protein in transgenic mouse livers. NAT1 is expressed ubiquitously and is extraordinarily conserved among species. It has homology to the carboxy-terminal portion of the eukaryotic translation initiation factor (eIF) 4G that binds eIF4A and eIF4E to form eIF4F. NAT1 binds eIF4A but not eIF4E and inhibits both cap-dependent and cap-independent translation. NAT1 is likely to be a fundamental translational repressor, and its aberrant editing could contribute to the potent oncogenesis induced by overexpression of APOBEC-1.