DNA damage processing at telomeres: The ends justify the means
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- 作者：Elise Fouquerel ; Dhvani Parikh ; Patricia Opresko ; plo4@pitt.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：6-4PP ; pyrimidine (6&ndash ; 4) pyrimidine photoproducts ; ALT ; alternative lengthening of telomeres ; BER ; base excision repair ; CPD ; cyclobutane pyrimidine dimer ; DDR ; DNAdamage response ; DSB ; DNA double strand break ; dsDNA ; double stranded DNA ; G4 ; G-quadruplex ; GGR ; global genome repair ; γH2AX ; phosphorylated histone H2AX ; HJ ; Holliday junction ; HR ; homologous recombination ; NER ; nucleotide excision repair ; NHEJ ; nonhomologous end joining ; ROS ; reactive oxygen species ; SCE ; sister chromatid exch
- 刊名：DNA Repair
- 出版年：2016
- 出版时间：August 2016
- 年：2016
- 卷：44
- 期：Complete
- 页码：159-168
- 全文大小：1924 K
文摘
Telomeres at chromosome ends are nucleoprotein structures consisting of tandem TTAGGG repeats and a complex of proteins termed shelterin. DNA damage and repair at telomeres is uniquely influenced by the ability of telomeric DNA to form alternate structures including loops and G-quadruplexes, coupled with the ability of shelterin proteins to interact with and regulate enzymes in every known DNA repair pathway. The role of shelterin proteins in preventing telomeric ends from being falsely recognized and processed as DNA double strand breaks is well established. Here we focus instead on recent developments in understanding the roles of shelterin proteins and telomeric DNA sequence and structure in processing genuine damage at telomeres induced by endogenous and exogenous DNA damage agents. We will highlight advances in double strand break repair, base excision repair and nucleotide excision repair at telomeres, and will discuss important questions remaining in the field.