KIN17, a mouse nuclear protein, binds to bent DNA fragments that are found at illegitimate recombination junctions in mammalian cells.
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.
Mazin
A
A
Groupe d'Etude Mutagenèse et Cancérogenèse, Institut Curie-Biologie, Centre Universitaire, Orsay, France.
Milot
E
E
Devoret
R
R
Chartrand
P
P
D000818:Animals; D002478:Cells, Cultured; D004247:DNA / Q000378:metabolism*; D004268:DNA-Binding Proteins / Q000378:metabolism*; D015321:Gene Rearrangement; D051379:Mice; D009687:Nuclear Proteins / Q000378:metabolism*; D009690:Nucleic Acid Conformation; D011485:Protein Binding; D011995:Recombination, Genetic
D004268:DNA-Binding Proteins; D009687:Nuclear Proteins; C071214:Kin protein, mouse; D004247:DNA