| First Author | Millar CB | Year | 2002 |
| Journal | Science | Volume | 297 |
| Issue | 5580 | Pages | 403-5 |
| PubMed ID | 12130785 | Mgi Jnum | J:77896 |
| Mgi Id | MGI:2182872 | Doi | 10.1126/science.1073354 |
| Citation | Millar CB, et al. (2002) Enhanced CpG mutability and tumorigenesis in MBD4-deficient mice. Science 297(5580):403-5 |
| abstractText | The mammalian protein MBD4 contains a methyl-CpG binding domain and can enzymatically remove thymine (T) or uracil (U) from a mismatched CpG site in vitro. These properties suggest that MBD4 might function in vivo to minimize the mutability of 5-methylcytosine by removing its deamination product from DNA. We tested this hypothesis by analyzing Mbd4-/- mice and found that the frequency of of C --> T transitions at CpG sites was increased by a factor of three. On a cancer-susceptible Apc(Min/+) background, Mbd4-/- mice showed accelerated tumor formation with CpG --> TpG mutations in the Apc gene. Thus MBD4 suppresses CpG mutability and tumorigenesis in vivo. |
