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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2018.10
- 수록면
- 297 - 302 (6page)
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초록· 키워드
오류제보하기
Cells are constantly exposed to endogenous and exogenous chemical and physical agents that damage their genome by forming DNA lesions. These lesions interfere with the normal functions of DNA such as transcription and replication, and need to be either repaired or tolerated. DNA lesions are accurately removed via various repair pathways. In contrast, tolerance mechanisms do not remove lesions but only allow replication to proceed despite the presence of unrepaired lesions. Cells possess two major tolerance strategies, namely translesion synthesis (TLS), which is an error-prone strategy and an accurate strategy based on homologous recombination (homologydependent gap repair [HDGR]). Thus, the mutation frequency reflects the relative extent to which the two tolerance pathways operate in vivo. In the present paper, we review the present understanding of the mechanisms of TLS and HDGR and propose a novel and comprehensive view of the way both strategies interact and are regulated in vivo.
목차
Abstract
INTRODUCTION
INTERPLAY BETWEEN NER AND REPLICATION IN A WILD-TYPE STRAIN FOLLOWING UV IRRADIATION
POST REPLICATIVE GAP REPAIR : INTERPLAY BETWEEN TLS AND HDGR
INTEGRATED MECHANISM OF TLS IN VIVO
INTERPLAY BETWEEN HDGR AND TLS : HOW HDGR IS MEASURED
CHRONOLOGICAL IMPLEMENTATION OF TLS AND HDGR
REFERENCES
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UCI(KEPA) : I410-ECN-0101-2018-513-003589336