| First Author | Koyanagi-Katsuta R | Year | 2002 |
| Journal | J Biochem | Volume | 131 |
| Issue | 6 | Pages | 833-7 |
| PubMed ID | 12038979 | Mgi Jnum | J:220883 |
| Mgi Id | MGI:5636813 | Doi | 10.1093/oxfordjournals.jbchem.a003172 |
| Citation | Koyanagi-Katsuta R, et al. (2002) Embryonic lethality of mutant mice deficient in the p116 gene. J Biochem 131(6):833-7 |
| abstractText | We report a lethal phenotype of mouse embryo with a disruption in the gene encoding p116, a subunit of the translation initiation factor, eIF3. The amino acid sequence of mouse p116, as deduced from the cDNA, shows high homology (97%) with human p116, and contains the conserved RNA binding sites, RNP1 and RNP2. The p116 mRNA is ubiquitously expressed in various organs, suggesting a house-keeping function of the p116 protein. To obtain genetic evidence for the essential role of the p116 protein in mouse cells, we constructed mice with a disruption in the p116 gene. Heterozygous p116(+/-) mice were intercrossed, and the genotypes of the offspring were determined. The results indicated no p116(-/-) pups among 84 neonates. Also, there were no p116(-/-) embryos 13.5 days postcoitum (d.p.c.). Among 77 embryos, there was only one p116(-/-) embryo at the blastocyst stage (3.5 d.p.c.). These results indicate that p116 plays an essential role in the early stages of mouse development. |
