| First Author | Peters AC | Year | 2003 |
| Journal | DNA Repair (Amst) | Volume | 2 |
| Issue | 4 | Pages | 427-35 |
| PubMed ID | 12606123 | Mgi Jnum | J:82381 |
| Mgi Id | MGI:2652917 | Doi | 10.1016/s1568-7864(03)00003-x |
| Citation | Peters AC, et al. (2003) Mammalian DNA mismatch repair protects cells from UVB-induced DNA damage by facilitating apoptosis and p53 activation. DNA Repair (Amst) 2(4):427-35 |
| abstractText | DNA mismatch repair (MMR) is integral to the maintenance of genomic stability and more recently has been demonstrated to affect apoptosis and cell cycle arrest in response to a variety of adducts induced by exogenous agents. Comparing Msh2-null and wildtype mouse embryonic fibroblasts (MEFs), both primary and transformed, we show that Msh2 deficiency results in increased survival post-UVB, and that UVB-induced apoptosis is significantly reduced in Msh2-deficient cells. Furthermore, p53 phosphorylation at serine 15 is delayed or diminished in Msh2-deficient cells, suggesting that Msh2 may act upstream of p53 in a post-UVB apoptosis or growth arrest response pathway. Taken together, these data suggest that MMR heterodimers containing Msh2 may function as a sensor of UVB-induced DNA damage and influence the initiation of UVB-induced apoptosis, thus implicating MMR in protecting against UV-induced tumorigenesis. |
