| First Author | Mazin A | Year | 1994 |
| Journal | Mol Gen Genet | Volume | 244 |
| Issue | 4 | Pages | 435-8 |
| PubMed ID | 8078469 | Mgi Jnum | J:20426 |
| Mgi Id | MGI:68515 | Doi | 10.1007/BF00286696 |
| Citation | Mazin A, et al. (1994) KIN17, a mouse nuclear protein, binds to bent DNA fragments that are found at illegitimate recombination junctions in mammalian cells. Mol Gen Genet 244(4):435-8 |
| abstractText | Illegitimate recombination is the dominant mechanism of recombination in mammalian somatic cells. It is responsible for most genome rearrangements such as translocations, deletions and integrations. Little is known as yet about the mechanism of illegitimate recombination and the enzymes involved. Recently, it has been shown that intrinsically bent DNA, also known as curved DNA, is present at chromosomal sites of illegitimate recombination events. Here we report that KIN17, a new mouse nuclear protein, binds to the curved DNA fragments found at illegitimate recombination sites. |
