DNA修复

       　DNA修复（DNA repairing）是细胞对DNA受损伤后的一种反应，这种反应可能使DNA结构恢复原样，重新能执行它原来的功能；但有时并非能完全消除DNA的损伤，只是使细胞能够耐受这DNA的损伤而能继续生存。也许这未能完全修复而存留下来的损伤会在适合的条件下显示出来（如细胞的癌变等），但如果细胞不具备这修复功能， 就无法对付经常在发生的DNA损伤事件，就不能生存。所以研究DNA修复也是探索生命的一个重要方面，而且与遗传疾病、肿瘤学等密切相关。对不同的DNA损伤，细胞可以有不同的修复反应。我们曾在220期做过相关报导。为此，CMBI特准备了关于DNA修复的特别报导，供大家参考。更多的文献，请用相关关键词通过CMBI文献查询获取。

• Structural Basis for the Methylation State-Specific Recognition of Histone H4-K20 by 53BP1 and Crb2 in DNA Repair
  
• Nucleotide excision repair and the ubiquitin proteasome pathway-Do all roads lead to Rome
  
• Major oxidative products of cytosine are substrates for the nucleotide incision repair pathway
  
• Drosophila homologs of FANCD2 and FANCL function in DNA repair
  
• Transpositions and translocations induced by site-specific double-strand breaks in budding yeast
  
• Topoisomerase II and the etiology of chromosomal translocations
  
• The involvement of non-B DNA structures in gross chromosomal rearrangements
  
• Telomeres and chromosome instability
  
• Studies on chromosome aberration induction
  
• Roles of nonhomologous DNA end joining, V(D)J recombination, and class switch recombination in chromosomal translocations
  
• Role of non-homologous end joining (NHEJ) in maintaining genomic integrity
  
• Recombination between retrotransposons as a source of chromosome rearrangements in the yeast Saccharomyces cerevisiae
  
• Recombinase, chromosomal translocations and lymphoid neoplasia
  
• Perspectives on the formation of radiation-induced exchange aberrations
  
• Pathways that suppress programmed DNA breaks from progressing to chromosomal breaks and translocations
  
• Palindromes and genomic stress fractures
  
• Palindrome-mediated chromosomal translocations in humans
  
• Myc translocations in B cell and plasma cell neoplasms
  
• Molecular processes of chromosome 9p21 deletions causing inactivation of the p16 tumor suppressor gene in human cancer
  
• Mechanisms of chromosomal translocation special issue of DNA Repair
  
• Etoposide and illegitimate DNA double-strand break repair in the generation of MLL translocations
  
• DNA double-strand break repair and chromosome translocations
  
• Distinguishing primary and secondary translocations in multiple myeloma
  
• Differential usage of non-homologous end-joining and homologous recombination in double strand break repair
  
• Dedicated to the core-Understanding the Fanconi anemia complex
  
• Contribution of DNA repair and cell cycle checkpoint arrest to the maintenance of genomic stability
  
• Common fragile sites as targets for chromosome rearrangements
  
• Chromosomal translocations involving the MLL gene
  
• Chromatin structural elements and chromosomal translocations in leukemia
  
• Biochemical mechanisms of chromosomal translocations resulting from DNA double-strand breaks
  
• Analysis of mutagenic V(D)J recombinase mediated mutations at the HPRT locus as an in vivo model for studying rearrangements with leukemogenic potential in children
  
• AID and Igh switch region-Myc chromosomal translocations
  
• Distinct roles for double-strand break repair pathways in translocation formation in mammalian cells
  
• Ntg1p, the base excision repair protein, generates mutagenic intermediates in yeast mitochondrial DNA
  
• MTH1, an oxidized purine nucleoside triphosphatase, prevents the cytotoxicity and neurotoxicity of oxidized purine nucleotides
  
• Analyses of the interaction of WRNIP1 with Werner syndrome protein (WRN) in vitro and in the cell
  
• Rad33, a new factor involved in nucleotide excision repair in Saccharomyces cerevisae
  
• Poor base stacking at DNA lesions may initiate recognition by many repair proteins
  
• Magnesium influences the discrimination and release of ADP by human RAD51
  
• Histone H2A phosphorylation and H3 methylation are required for a novel Rad9 DSB repair function following checkpoint activation
  
• Genomic instability due to V(D)J recombination-associated transposition
  
• Defining the salt effect on human RAD51 activities
  
• A role for Mlh3 in somatic hypermutation
  
• Focus on recombinational DNA repair
  
• Tails of histones lost
  
• γH2AX and MDC1
  
• Topoisomerase deficiencies subtly enhance global genomic repair of ultraviolet-induced DNA damage in Saccharomyces cerevisiae
  
• Roles of DNA ligase III and XRCC1 in regulating the switch between short patch and long patch BER
  
• DNA-PK phosphorylates histone H2AX during apoptotic DNA fragmentation in mammalian cells
  
• Cellular responses to DNA damage
  
• Mutagenesis and the three R's in yeast
  
• Atmnd1-Δ1 is sensitive to gamma-irradiation and defective in meiotic DNA repair
  
• Role of mitochondrial DNA in toxic responses to oxidative stress
  
• Recent advances in understanding of the DNA double-strand break repair machinery of plants
  
• Analysis of interaction between DNA and Deinococcus radiodurans PprA protein by Atomic force microscopy
  
• Ku-A multifunctional protein involved in telomere maintenance
  
• Identification and functional analysis of TopBP1 and its homologs
  
• Cellular machineries for chromosomal DNA repair
  
• Focus on recombinational DNA repair
  
• Specificity of Protein Interactions Mediated by BRCT Domains of the XRCC1 DNA Repair Protein
  
• Histone H2A phosphorylation in DNA double-strand break repair