본문 바로가기
HOME> 논문 > 논문 검색상세

논문 상세정보

Nucleic acids research v.45 no.2, 2017년, pp.739 - 748   SCI SCIE
본 등재정보는 저널의 등재정보를 참고하여 보여주는 베타서비스로 정확한 논문의 등재여부는 등재기관에 확인하시기 바랍니다.

Regulation of oxidized base damage repair by chromatin assembly factor 1 subunit A

Yang, Chunying (Department of Radiation Oncology, Houston Methodist Research Institute, Houston, TX 77030, USA ); Sengupta, Shiladitya (Department of Radiation Oncology, Houston Methodist Research Institute, Houston, TX 77030, USA ); Hegde, Pavana M. (Department of Radiation Oncology, Houston Methodist Research Institute, Houston, TX 77030, USA ); Mitra, Joy (Department of Radiation Oncology, Houston Methodist Research Institute, Houston, TX 77030, USA ); Jiang, Shuai (Biological Systems and Engineering Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA ); Holey, Brooke (Biological Systems and Engineering Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA ); Sarker, Altaf H. (Biological Systems and Engineering Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA ); Tsai, Miaw-Sheue (Biological Systems and Engineering Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA ); Hegde, Muralidhar L. (Department of Radiation Oncology, Houston Methodist Research Institute, Houston, TX 77030, USA ); Mitra, Sankar (Department of Radiation Oncology, Houston Methodist Research Institute, Hou );
  • 초록  

    Reactive oxygen species (ROS), generated both endogenously and in response to exogenous stress, induce point mutations by mis-replication of oxidized bases and other lesions in the genome. Repair of these lesions via base excision repair (BER) pathway maintains genomic fidelity. Regulation of the BER pathway for mutagenic oxidized bases, initiated by NEIL1 and other DNA glycosylases at the chromatin level remains unexplored. Whether single nucleotide (SN)-BER of a damaged base requires histone deposition or nucleosome remodeling is unknown, unlike nucleosome reassembly which is shown to be required for other DNA repair processes. Here we show that chromatin assembly factor (CAF)-1 subunit A (CHAF1A), the p150 subunit of the histone H3/H4 chaperone, and its partner anti-silencing function protein 1A (ASF1A), which we identified in human NEIL1 immunoprecipitation complex, transiently dissociate from chromatin bound NEIL1 complex in G1 cells after induction of oxidative base damage. CHAF1A inhibits NEIL1 initiated repair in vitro . Subsequent restoration of the chaperone-BER complex in cell , presumably after completion of repair, suggests that histone chaperones sequester the repair complex for oxidized bases in non-replicating chromatin, and allow repair when oxidized bases are induced in the genome.


 활용도 분석

  • 상세보기

    amChart 영역
  • 원문보기

    amChart 영역

원문보기

무료다운로드
유료다운로드

유료 다운로드의 경우 해당 사이트의 정책에 따라 신규 회원가입, 로그인, 유료 구매 등이 필요할 수 있습니다. 해당 사이트에서 발생하는 귀하의 모든 정보활동은 NDSL의 서비스 정책과 무관합니다.

원문복사신청을 하시면, 일부 해외 인쇄학술지의 경우 외국학술지지원센터(FRIC)에서
무료 원문복사 서비스를 제공합니다.

NDSL에서는 해당 원문을 복사서비스하고 있습니다. 위의 원문복사신청 또는 장바구니 담기를 통하여 원문복사서비스 이용이 가능합니다.

이 논문과 함께 출판된 논문 + 더보기