DNA Repair

       　环境和生物体内的因素都经常会导致DNA的结构发生改变。这些改变可能影响生物细胞的功能和遗传特性，导致三种独立的结果：1.细胞死亡； 2. 使细胞获得新的功能或进化； 3.使细胞只有DNA结构的遗传性改变而没有表型变化。这些变化的结果因DNA结构变化的部位、类型和范围不同而异。 生物在进化过程中获得的DNA修复功能，对生物的生存和维持遗传的稳定性是至关重要的。对有些DNA的损伤，细胞能将其完全修复到原样，如可将嘧啶二聚体切开、DNA单链断裂可重新连接、碱基缺失可再配对插入、加成的烷基可以移除、一条链上的碱基或核苷酸的错误可以切除并依赖互补链作模板而复制重新修复等。对DNA较严重的损伤，细胞可采取重组修复、SOS修复等方式进行反应，以期提高细胞的存活率，但不能完全消除DNA的损伤，会带给细胞较高的突变率。
       　DNA的损伤和修复与遗传、突变、寿命、衰老、辐射效应、肿瘤发生、某些毒剂的作用、以及某些遗传性疾病等有密切的关系。目前对DNA损伤修复的认识还不透彻。为此CMBI特准备了关于DNA Repair的特别报道，供实践参考。更多文献,请用相关关键词通过CMBI文献查询获取。

• DNA Repair
  
• 53BP1, an activator of ATM in response to DNA damage
  
• Ageing and PARP
  
• Alkylation damage in DNA and RNA—repair mechanisms and medical significance
  
• Ataxia–telangiectasia, an evolving phenotype
  
• Ataxia-telangiectasia-like disorder (ATLD)—its clinical presentation and molecular basis
  
• Biochemical characterization of the ataxia-telangiectasia mutated (ATM) protein from human cells
  
• Characterization of palindromic loop mismatch repair tracts in mammalian cells
  
• Chk1 in the DNA damage response
  
• Chk2 protein kinase
  
• Chromosome damage and progression into and through mitosis in vertebrates
  
• Claspin, a regulator of Chk1 in DNA replication stress pathway
  
• clinical manifestation of defective response to DNA double-strand breaks
  
• Constitutively active DNA damage checkpoint pathways as the driving force for the high frequency of p53 mutations in human cancer
  
• DNA damage responses to oxidative stress
  
• Defining the biochemistry of mismatch repair
  
• Dial 9–1–1 for DNA damage
  
• DNA damage recognition and repair by the murine MutY homologue
  
• DNA damage-induced activation of ATM and ATM-dependent signaling pathways
  
• DNA double-strand break response in the nervous system
  
• DNA double-strand break response pathway
  
• DNA recombination, chromosomal stability and carcinogenesis
  
• DNA single-strand breaks and neurodegeneration
  
• DSB repair-the yeast paradigm
  
• Dysfunctional mammalian telomeres join with DNA double-strand breaks
  
• Early thinking on the nature of mismatch repair
  
• emerging role of E2F-1 in the DNA damage response and checkpoint control
  
• Error-prone DNA repair and translesion DNA synthesis
  
• EXO1-A multi-tasking eukaryotic nuclease
  
• First US–EU DNA Repair Meeting
  
• Functional consequences of sequence alterations in the ATM gene
  
• Genetic biomarkers of therapeutic radiation sensitivity
  
• gt-Activation of stress-responsive promoters by ionizing radiation for deployment in targeted gene therapy
  
• H2AX-the histone guardian of the genome
  
• High frequency of nucleotide misincorporations upon the processing of double-strand breaks
  
• High G-C content of cohesive overhangs renders DNA end joining Ku-independent
  
• Homologous recombination-mediated double-strand break repair
  
• Impact of mitochondria on nuclear genome stability
  
• Inroads into base excision repair I
  
• Inroads into base excision repair II
  
• Interactions of viruses with the cellular DNA repair machinery
  
• Interplay between chromatin and cell cycle checkpoints in the context of ATR-ATM-dependent checkpoints
  
• interplay of Fanconi anemia proteins in the DNA damage response
  
• Mammalian cell cycle checkpoints-signalling pathways and their organization in space and time
  
• MDC1-NFBD1-a key regulator of the DNA damage response in higher eukaryotes
  
• Mechanism of DNA double-strand break repair by non-homologous end joining
  
• mechanism of non-homologous end-joining
  
• mechanism of vertebrate nonhomologous DNA end joining and its role in V(D)J recombination
  
• Mechanisms of DNA damage recognition and strand discrimination in human nucleotide excision repair
  
• Mending human genes
  
• Mismatch repair and DNA damage signalling
  
• Mre11 complex and ATM-a two-way functional interaction in recognising and signaling DNA double strand breaks
  
• multifaceted role of mTOR in cellular stress responses
  
• NBS1 and its functional role in the DNA damage response
  
• Network responses to DNA damaging agents
  
• overview of three new disorders associated with genetic instability
  
• PARP-1, PARP-2 and ATM in the DNA damage response
  
• PI 3-kinase related kinases-‘big’ players in stress-induced signaling pathways
  
• Pre-isotopic and post-isotopic eras of DNA repair
  
• programmed damage and repair
  
• Regulation of DNA replication by ATR
  
• Relevance and irrelevance of DNA damage response to radiotherapy
  
• Replication Protein A phosphorylation and the cellular response to DNA damage
  
• Replication Protein A phosphorylation and the cellular response to DNA damageThe role of ATM and ATR in the cellular response to hypoxia and re-oxygenation
  
• Reverse genetic studies of the DNA damage response in the chicken B lymphocyte line DT40
  
• Role of DNA–PK in the cellular response to DNA double-strand breaks
  
• role of the DNA double-strand break response network in meiosis
  
• Structure and function of the double-strand break repair machinery
  
• Telomeres and the DNA damage response
  
• The ATM-related kinase, hSMG-1, bridges genome and RNA surveillance pathways
  
• The cellular response to general and programmed DNA double strand breaks
  
• The Elg1 replication factor C-like complex
  
• The Mre11 complex and the metabolism of chromosome breaks
  
• The p53 response to DNA damage
  
• The role of SMC proteins in the responses to DNA damage
  
• The switch from survival responses to apoptosis after chromosomal breaks
  
• The XRCC genes-expanding roles in DNA double-strand break repair
  
• Transcription and DNA adducts
  
• Molecular interaction map of the p53 and Mdm2 logic elements, which control the Off-On switch of p53 in response to DNA damage