Mutagenesis dependent upon the combination of activation-induced deaminase expression and a double-strand break.

[1]  J. Jiricny,et al.  Interference of mismatch and base excision repair during the processing of adjacent U/G mispairs may play a key role in somatic hypermutation , 2009, Proceedings of the National Academy of Sciences.

[2]  M. Goodman,et al.  Stochastic properties of processive cytidine DNA deaminases AID and APOBEC3G , 2009, Philosophical Transactions of the Royal Society B: Biological Sciences.

[3]  J. Haber,et al.  A recombination execution checkpoint regulates the choice of homologous recombination pathway during DNA double-strand break repair. , 2009, Genes & development.

[4]  D. Gordenin,et al.  The Transition of Closely Opposed Lesions to Double-Strand Breaks during Long-Patch Base Excision Repair Is Prevented by the Coordinated Action of DNA Polymerase δ and Rad27/Fen1 , 2008, Molecular and Cellular Biology.

[5]  D. Gordenin,et al.  Hypermutability of Damaged Single-Strand DNA Formed at Double-Strand Breaks and Uncapped Telomeres in Yeast Saccharomyces cerevisiae , 2008, PLoS genetics.

[6]  Sergio Roa,et al.  The biochemistry of somatic hypermutation. , 2008, Annual review of immunology.

[7]  M. Neuberger,et al.  Dependence of antibody gene diversification on uracil excision , 2007, The Journal of experimental medicine.

[8]  D. Schatz,et al.  Activation-induced Cytidine Deaminase-mediated Sequence Diversification Is Transiently Targeted to Newly Integrated DNA Substrates* , 2007, Journal of Biological Chemistry.

[9]  J. Haber,et al.  Break-induced replication and telomerase-independent telomere maintenance require Pol32 , 2007, Nature.

[10]  A. Aguilera,et al.  Activation-induced cytidine deaminase action is strongly stimulated by mutations of the THO complex , 2007, Proceedings of the National Academy of Sciences.

[11]  S. Takeda,et al.  DNA-Dependent Protein Kinase Inhibits AID-Induced Antibody Gene Conversion , 2007, PLoS biology.

[12]  Samuel H. Wilson,et al.  Down-regulation of DNA polymerase beta accompanies somatic hypermutation in human BL2 cell lines. , 2007, DNA repair.

[13]  M. Neuberger,et al.  Somatic hypermutation: activation-induced deaminase for C/G followed by polymerase η for A/T , 2007, The Journal of experimental medicine.

[14]  M. Neuberger,et al.  The in vivo pattern of AID targeting to immunoglobulin switch regions deduced from mutation spectra in msh2 −/− ung −/− mice , 2006, The Journal of experimental medicine.

[15]  J. Strathern,et al.  Homologous recombination is promoted by translesion polymerase poleta. , 2005, Molecular cell.

[16]  Samuel H. Wilson,et al.  REV1 mediated mutagenesis in base excision repair deficient mouse fibroblast. , 2005, DNA repair.

[17]  P. Casali,et al.  DNA Lesions and Repair in Immunoglobulin Class Switch Recombination and Somatic Hypermutation , 2005, Annals of the New York Academy of Sciences.

[18]  K. Sugimoto,et al.  Requirement of the Mre11 Complex and Exonuclease 1 for Activation of the Mec1 Signaling Pathway , 2004, Molecular and Cellular Biology.

[19]  M. Neuberger,et al.  Mismatch recognition and uracil excision provide complementary paths to both Ig switching and the A/T-focused phase of somatic mutation. , 2004, Molecular cell.

[20]  Samuel H. Wilson,et al.  Recombinogenic Phenotype of Human Activation-Induced Cytosine Deaminase , 2004, The Journal of Immunology.

[21]  P. Sung,et al.  Role of the nuclease activity of Saccharomyces cerevisiae Mre11 in repair of DNA double-strand breaks in mitotic cells. , 2004, Genetics.

[22]  L. Boursier,et al.  Analysis of strand biased 'G'.C hypermutation in human immunoglobulin V(lambda) gene segments suggests that both DNA strands are targets for deamination by activation-induced cytidine deaminase. , 2004, Molecular immunology.

[23]  J. Strathern,et al.  Error-prone DNA polymerases: when making a mistake is the only way to get ahead. , 2003, Annual review of genetics.

[24]  Samuel H. Wilson,et al.  Base Excision Repair Intermediates Induce p53-independent Cytotoxic and Genotoxic Responses* , 2003, Journal of Biological Chemistry.

[25]  M. Goodman,et al.  Processive AID-catalysed cytosine deamination on single-stranded DNA simulates somatic hypermutation , 2003, Nature.

[26]  Reuben S Harris,et al.  Immunity through DNA deamination. , 2003, Trends in biochemical sciences.

[27]  M. Goodman,et al.  Activation-induced cytidine deaminase deaminates deoxycytidine on single-stranded DNA but requires the action of RNase , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[28]  D. Barnes,et al.  Immunoglobulin Isotype Switching Is Inhibited and Somatic Hypermutation Perturbed in UNG-Deficient Mice , 2002, Current Biology.

[29]  M. Neuberger,et al.  AID mutates E. coli suggesting a DNA deamination mechanism for antibody diversification , 2002, Nature.

[30]  Samuel H. Wilson,et al.  Mutations associated with base excision repair deficiency and methylation-induced genotoxic stress , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[31]  T. Honjo,et al.  The AID enzyme induces class switch recombination in fibroblasts , 2002, Nature.

[32]  M. Neuberger,et al.  AID Is Essential for Immunoglobulin V Gene Conversion in a Cultured B Cell Line , 2002, Current Biology.

[33]  Alberto Martin,et al.  Activation-induced cytidine deaminase turns on somatic hypermutation in hybridomas , 2002, Nature.

[34]  M. Goodman,et al.  Error-Prone Candidates Vie for Somatic Mutation , 2000, The Journal of experimental medicine.

[35]  D. Schatz,et al.  Cell-cycle-regulated DNA double-strand breaks in somatic hypermutation of immunoglobulin genes , 2000, Nature.

[36]  K. Rajewsky,et al.  DNA double-strand breaks in immunoglobulin genes undergoing somatic hypermutation. , 2000, Immunity.

[37]  T. Honjo,et al.  Class Switch Recombination and Hypermutation Require Activation-Induced Cytidine Deaminase (AID), a Potential RNA Editing Enzyme , 2000, Cell.

[38]  A. Fischer,et al.  Activation-Induced Cytidine Deaminase (AID) Deficiency Causes the Autosomal Recessive Form of the Hyper-IgM Syndrome (HIGM2) , 2000, Cell.

[39]  W. Edelmann,et al.  Somatic Hypermutation in Muts Homologue (Msh)3-, Msh6-, and Msh3/Msh6-Deficient Mice Reveals a Role for the Msh2–Msh6 Heterodimer in Modulating the Base Substitution Pattern , 2000, The Journal of experimental medicine.

[40]  T. Lindahl,et al.  Quality control by DNA repair. , 1999, Science.

[41]  V. Poltoratsky,et al.  The Promotion of  V Region Hypermutation , 1997, The Journal of experimental medicine.

[42]  K. Rajewsky.  Clonal selection and learning in the antibody system , 1996, Nature.

[43]  N. Maizels,et al.  Somatic hypermutation: How many mechanisms diversify V region sequences? , 1995, Cell.

[44]  H. Krokan,et al.  Properties of a recombinant human uracil-DNA glycosylase from the UNG gene and evidence that UNG encodes the major uracil-DNA glycosylase. , 1995, Biochemistry.

[45]  N A Kolchanov,et al.  Somatic hypermutagenesis in immunoglobulin genes. II. Influence of neighbouring base sequences on mutagenesis. , 1992, Biochimica et biophysica acta.

[46]  R. Laskov,et al.  The role of somatic hypermutation in the generation of antibody diversity. , 1989, Science.

[47]  F. Alt,et al.  Development of the primary antibody repertoire. , 1987, Science.

[48]  A Cumano,et al.  Evolutionary and somatic selection of the antibody repertoire in the mouse. , 1987, Science.

[49]  J. S. Maritz,et al.  A Note on Estimating the Variance of the Sample Median , 1978 .

[50]  D. Groggel.  Practical Nonparametric Statistics , 1972, Technometrics.

[51]  S. Brenner,et al.  Origin of Antibody Variation , 1966, Nature.

[52]  Francesca Storici,et al.  The delitto perfetto approach to in vivo site-directed mutagenesis and chromosome rearrangements with synthetic oligonucleotides in yeast. , 2006, Methods in enzymology.

[53]  C. Woo,et al.  The generation of antibody diversity through somatic hypermutation and class switch recombination. , 2004, Genes & development.