Antibody diversification caused by disrupted mismatch repair and promiscuous DNA polymerases

Class Switch Recombination and Hypermutation Require Activation-Induced Cytidine Deaminase (AID), a Potential RNA Editing Enzyme

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RAD6-dependent DNA repair is linked to modification of PCNA by ubiquitin and SUMO

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Activation-Induced Cytidine Deaminase (AID) Deficiency Causes the Autosomal Recessive Form of the Hyper-IgM Syndrome (HIGM2)

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Specific Expression of Activation-induced Cytidine Deaminase (AID), a Novel Member of the RNA-editing Deaminase Family in Germinal Center B Cells

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Mechanism and Regulation of Class Switch Recombination

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AID mutates E. coli suggesting a DNA deamination mechanism for antibody diversification

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Immunoglobulin Isotype Switching Is Inhibited and Somatic Hypermutation Perturbed in UNG-Deficient Mice

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Endonucleolytic Function of MutLα in Human Mismatch Repair

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Class-switch recombination: interplay of transcription, DNA deamination and DNA repair

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RNA Editing Enzyme APOBEC1 and Some of Its Homologs Can Act as DNA Mutators

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IgH class switching and translocations use a robust non-classical end-joining pathway

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Regulation of monoubiquitinated PCNA by DUB autocleavage

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Mismatch Recognition and Uracil Excision Provide Complementary Paths to Both Ig Switching and the A/T-Focused Phase of Somatic Mutation

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DNA polymerase η is an A-T mutator in somatic hypermutation of immunoglobulin variable genes

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Targeting of somatic hypermutation

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Hot Spot Focusing of Somatic Hypermutation in MSH2-Deficient Mice Suggests Two Stages of Mutational Targeting

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Boundaries of somatic mutation in rearranged immunoglobulin genes: 5' boundary is near the promoter, and 3' boundary is approximately 1 kb from V(D)J gene.

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Error-free and error-prone lesion bypass by human DNA polymerase kappa in vitro

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Somatic mutation hotspots correlate with DNA polymerase η error spectrum

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53BP1 regulates DNA resection and the choice between classical and alternative end joining during class switch recombination

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Classical and Alternative End-Joining Pathways for Repair of Lymphocyte-Specific and General DNA Double-Strand Breaks

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Altered somatic hypermutation and reduced class-switch recombination in exonuclease 1–mutant mice

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Deficiency in Msh2 affects the efficiency and local sequence specificity of immunoglobulin class‐switch recombination: parallels with somatic hypermutation

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Fidelity and Processivity of DNA Synthesis by DNA Polymerase κ, the Product of the Human DINB1 Gene

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Reduced Isotype Switching in Splenic B Cells from Mice Deficient in Mismatch Repair Enzymes

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AID and Somatic Hypermutation

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Strand-biased defect in C/G transversions in hypermutating immunoglobulin genes in Rev1-deficient mice

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MSH2–MSH6 stimulates DNA polymerase η, suggesting a role for A:T mutations in antibody genes

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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

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APE1- and APE2-dependent DNA breaks in immunoglobulin class switch recombination

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DNA polymerase η is the sole contributor of A/T modifications during immunoglobulin gene hypermutation in the mouse

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AID-dependent somatic hypermutation occurs as a DNA single-strand event in the BL2 cell line

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The in vivo pattern of AID targeting to immunoglobulin switch regions deduced from mutation spectra in msh2 −/− ung −/− mice

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Increased Hypermutation at G and C Nucleotides in Immunoglobulin Variable Genes from Mice Deficient in the MSH2 Mismatch Repair Protein

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129-derived Strains of Mice Are Deficient in DNA Polymerase ι and Have Normal Immunoglobulin Hypermutation

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Error rate and specificity of human and murine DNA polymerase η

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A Role for PCNA Ubiquitination in Immunoglobulin Hypermutation

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A Role for Msh6 But Not Msh3 in Somatic Hypermutation and Class Switch Recombination

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A/T mutagenesis in hypermutated immunoglobulin genes strongly depends on PCNAK164 modification

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Activation-Induced Cytidine Deaminase-Dependent DNA Breaks in Class Switch Recombination Occur during G1 Phase of the Cell Cycle and Depend upon Mismatch Repair

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Mismatch Repair Deficiency Interferes with the Accumulation of Mutations in Chronically Stimulated B Cells and Not with the Hypermutation Process

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Switch junction sequences in PMS2-deficient mice reveal a microhomology-mediated mechanism of Ig class switch recombination

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Uracil residues dependent on the deaminase AID in immunoglobulin gene variable and switch regions

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Repair of radiation induced DNA double strand breaks by backup NHEJ is enhanced in G2

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A Portable Hot Spot Recognition Loop Transfers Sequence Preferences from APOBEC Family Members to Activation-induced Cytidine Deaminase

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PCNA Ubiquitination Is Important, But Not Essential for Translesion DNA Synthesis in Mammalian Cells

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DNA Polymerase η Is Involved in Hypermutation Occurring during Immunoglobulin Class Switch Recombination

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Cutting Edge: DNA Polymerases μ and λ Are Dispensable for Ig Gene Hypermutation

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Somatic Hypermutation and Class Switch Recombination in Msh6−/−Ung−/− Double-Knockout Mice

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Different mutation signatures in DNA polymerase η- and MSH6-deficient mice suggest separate roles in antibody diversification

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Ubiquitylated PCNA plays a role in somatic hypermutation and class-switch recombination and is required for meiotic progression

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The IgH 3′ regulatory region controls somatic hypermutation in germinal center B cells

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Altered spectra of hypermutation in antibodies from mice deficient for the DNA mismatch repair protein PMS2

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Mismatch repair converts AID-instigated nicks to double-strand breaks for antibody class-switch recombination

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Msh2 ATPase Activity Is Essential for Somatic Hypermutation at A-T Basepairs and for Efficient Class Switch Recombination

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Examination of Msh6- and Msh3-deficient Mice in Class Switching Reveals Overlapping and Distinct Roles of MutS Homologues in Antibody Diversification

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Mice reconstituted with DNA polymerase β-deficient fetal liver cells are able to mount a T cell-dependent immune response and mutate their Ig genes normally

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Distinctive characteristics of germinal center B cells

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Local Sequence Targeting in the AID/APOBEC Family Differentially Impacts Retroviral Restriction and Antibody Diversification

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Effects of Sequence and Structure on the Hypermutability of Immunoglobulin Genes

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PMS2 endonuclease activity has distinct biological functions and is essential for genome maintenance

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Mammalian Exo1 encodes both structural and catalytic functions that play distinct roles in essential biological processes

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Human MSH6 Deficiency Is Associated with Impaired Antibody Maturation

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DNA Polymerase η Contributes to Strand Bias of Mutations of A versus T in Immunoglobulin Genes

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Absence of DNA Polymerase η Reveals Targeting of C Mutations on the Nontranscribed Strand in Immunoglobulin Switch Regions

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Somatic hypermutation: activation-induced deaminase for C/G followed by polymerase η for A/T

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AIDing antibody diversity by error-prone mismatch repair

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Switch recombination and somatic hypermutation are controlled by the heavy chain 3′ enhancer region

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DNA Polymerases η and θ Function in the Same Genetic Pathway to Generate Mutations at A/T during Somatic Hypermutation of Ig Genes

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The Role of Activation‐Induced Deaminase in Antibody Diversification and Chromosome Translocations

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Epigenetic targeting of activation-induced cytidine deaminase

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Spt5 accumulation at variable genes distinguishes somatic hypermutation in germinal center B cells from ex vivo–activated cells

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Hypermutation in Ig V genes from mice deficient in the MLH1 mismatch repair protein.

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Differential expression of APE1 and APE2 in germinal centers promotes error-prone repair and A:T mutations during somatic hypermutation

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Mlh1 Can Function in Antibody Class Switch Recombination Independently of Msh2

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Dependence of nucleotide substitutions on Ung2, Msh2, and PCNA-Ub during somatic hypermutation

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Attracting AID to targets of somatic hypermutation

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A Critical Role for REV1 in Regulating the Induction of C:G Transitions and A:T Mutations during Ig Gene Hypermutation

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Consequences of OX40-OX40 ligand interactions in Langerhans cell function: enhanced contact hypersensitivity responses in OX40L-transgenic mice

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Does DNA repair occur during somatic hypermutation?

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Strikingly different properties of uracil-DNA glycosylases UNG2 and SMUG1 may explain divergent roles in processing of genomic uracil

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Transcriptional pausing and stalling causes multiple clustered mutations by human activation‐induced deaminase

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Reevaluation of the role of DNA polymerase θ in somatic hypermutation of immunoglobulin genes

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PCNA ubiquitination-independent activation of polymerase η during somatic hypermutation and DNA damage tolerance

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DNA polymerase ζ generates tandem mutations in immunoglobulin variable regions

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The Mismatch Repair Protein Msh6 Influences the In Vivo AID Targeting to the Ig Locus

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DNA polymerases β and λ do not directly affect Ig variable region somatic hypermutation although their absence reduces the frequency of mutations

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DNA polymerase <b>η</b> mutational signatures are found in a variety of different types of cancer

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