| First Author | Shu Z | Year | 1999 |
| Journal | Mol Cell Biol | Volume | 19 |
| Issue | 12 | Pages | 8686-93 |
| PubMed ID | 10567591 | Mgi Jnum | J:58601 |
| Mgi Id | MGI:1349263 | Doi | 10.1128/mcb.19.12.8686 |
| Citation | Shu Z, et al. (1999) Disruption of muREC2/RAD51L1 in mice results in early embryonic lethality which can Be partially rescued in a p53(-/-) background. Mol Cell Biol 19(12):8686-93 |
| abstractText | muREC2/RAD51L1 is a radiation-inducible gene that regulates cell cycle progression. To elucidate the biological function of muREC2/RAD51L1, the gene was disrupted in embryonic stem cells by homologous recombination. Mice heterozygous for muREC2/RAD51L1 appear normal and fertile; however, no homozygous pups were born after interbreeding of heterozygous mice. Timed pregnancy studies showed that homozygous mutant embryos were severely retarded in growth as early as ca. 5 days gestation (E5.5) and were completely resorbed by E8.5. Mutant blastocyst outgrowth was also severely impaired in a double-knockout embryo, but embryonic development did progress further in a p53-null background. These results suggest that muREC2/RAD51L1 plays a role in cell proliferation and early embryonic development, perhaps through interaction with p53. |
