| First Author | Nilsen H | Year | 2000 |
| Journal | Mol Cell | Volume | 5 |
| Issue | 6 | Pages | 1059-65 |
| PubMed ID | 10912000 | Mgi Jnum | J:63056 |
| Mgi Id | MGI:1860377 | Doi | 10.1016/s1097-2765(00)80271-3 |
| Citation | Nilsen H, et al. (2000) Uracil-DNA glycosylase (UNG)-deficient mice reveal a primary role of the enzyme during DNA replication. Mol Cell 5(6):1059-65 |
| abstractText | Gene-targeted knockout mice have been generated lacking the major uracil-DNA glycosylase, UNG. In contrast to ung- mutants of bacteria and yeast, such mice do not exhibit a greatly increased spontaneous mutation frequency. However, there is only slow removal of uracil from misincorporated dUMP in isolated ung-/- nuclei and an elevated steady-state level of uracil in DNA in dividing ung-/- cells. A backup uracil-excising activity in tissue extracts from ung null mice, with properties indistinguishable from the mammalian SMUG1 DNA glycosylase, may account for the repair of premutagenic U:G mispairs resulting from cytosine deamination in vivo. The nuclear UNG protein has apparently evolved a specialized role in mammalian cells counteracting U:A base pairs formed by use of dUTP during DNA synthesis. |
