Repair of genomic interstrand crosslinks

被引：1
作者：
Bellani, Marina A. [1 ]
Shaik, Althaf [1 ]
Majumdar, Ishani [1 ]
Ling, Chen [1 ]
Seidman, Michael M. [1 ]
机构：
[1] Natl Inst Aging, NIH, Lab Mol Biol & Immunol, Baltimore, MD 21224 USA
来源：
DNA REPAIR | 2024年 / 141卷
关键词：
Interstrand crosslink; DNA repair; Unhooking; Cancer chemotherapy; Drug resistance; NUCLEOTIDE EXCISION-REPAIR; FANCONI-ANEMIA PATHWAY; TRANSCRIPTION-COUPLED REPAIR; DOUBLE-STRAND BREAKS; CELL LUNG-CANCER; DNA-REPAIR; ABASIC SITES; NITROGEN-MUSTARD; MISMATCH REPAIR; ESCHERICHIA-COLI;
D O I：
10.1016/j.dnarep.2024.103739
中图分类号：
Q3 [遗传学];
学科分类号：
071007 ; 090102 ;
摘要：
Genomic interstrand crosslinks (ICLs) are formed by reactive species generated during normal cellular metabolism, produced by the microbiome, and employed in cancer chemotherapy. While there are multiple options for replication dependent and independent ICL repair, the crucial step for each is unhooking one DNA strand from the other. Much of our insight into mechanisms of unhooking comes from powerful model systems based on plasmids with defined ICLs introduced into cells or cell free extracts. Here we describe the properties of exogenous and endogenous ICL forming compounds and provide an historical perspective on early work on ICL repair. We discuss the modes of unhooking elucidated in the model systems, the concordance or lack thereof in drug resistant tumors, and the evolving view of DNA adducts, including ICLs, formed by metabolic aldehydes.
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页数：18
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