TAILIEUCHUNG - Báo cáo khoa học: Biochemical analysis of the human EVL domains in homologous recombination

EVL is a member of the ENA⁄VASP family, which is involved in actin-remodeling processes. Previously, we reported that human EVL directly interacts with RAD51, which is an essential protein in the homologous recombinational repair of DNA double-strand breaks, and stimulates RAD51-mediated recombination reactionsin vitro. | ỊFEBS Journal Biochemical analysis of the human EVL domains in homologous recombination Motoki Takaku Shinichi Machida Shugo Nakayama Daisuke Takahashi and Hitoshi Kurumizaka Laboratory of StructuralBiology Graduate Schoolof Advanced Science and Engineering Waseda University Tokyo Japan Keywords DSB ENA VASP EVL homologous recombination RAD51 Correspondence H. Kurumizaka Laboratory of Structural Biology Graduate Schoolof Advanced Science and Engineering Waseda University 2-2 Wakamatsu-cho Shinjuku-ku Tokyo 162-8480 Japan Fax 81 3 5367 2820 Tel 81 3 5369 7315 E-mail kurumizaka@ Received 3 June 2009 revised 3 August 2009 accepted 6 August 2009 doi EVL is a member of the ENA VASP family which is involved in actin-remodeling processes. Previously we reported that human EVL directly interacts with RAD51 which is an essential protein in the homologous recombinational repair of DNA double-strand breaks and stimulates RAD51-mediated recombination reactions in vitro. To identify the EVL domain required for the recombination function we purified the EVL fragments EVL 1-221 and EVL 222-418 which contain the EVH1 and Pro-rich domains and the EVH2 domain respectively. We found that EVL 222-418 possesses DNA-binding and RAD51-binding activities and also stimulates RAD51-mediated homologous pairing. In contrast EVL 1-221 did not exhibit any of these activities. Therefore the EVH2 domain which is highly conserved among the ENA VASP family proteins may be responsible for the recombination function of EVL. Structured digital abstract MINT-7239394 EVL uniprotkb Q9UI08 binds MI 0407 to RAD51 uniprotkb Q06609 by pull down MI 0096 Introduction Chromosomal DNA is constantly exposed to various DNA-damaging agents including ionizing radiation crosslinking reagents and oxidative stress. A doublestrand break DSB which is induced by such DNA-damaging agents and or failure of DNA replication results in chromosome aberrations and tumorigenesis if it is

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