RPA accumulation during class switch recombination represents 5'-3' DNA-end resection during the S-G2/M phase of the cell cycle.
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M. Nussenzweig | A. Nussenzweig | R. Casellas | D. Robbiani | E. Brown | Anne Bothmer | H. Nakahashi | W. Resch | Arito Yamane | Thiago Y. Oliveira | Philipp C. Rommel
[1] Nina M. Donghia,et al. Activation-Induced Cytidine Deaminase-Initiated Off-Target DNA Breaks Are Detected and Resolved during S Phase , 2012, The Journal of Immunology.
[2] Adrian L. Smith,et al. Ectopic restriction of DNA repair reveals that UNG2 excises AID-induced uracils predominantly or exclusively during G1 phase , 2012, The Journal of experimental medicine.
[3] Ty C. Voss,et al. DNA damage defines sites of recurrent chromosomal translocations in B lymphocytes , 2012, Nature.
[4] B. Helmink,et al. The response to and repair of RAG-mediated DNA double-strand breaks. , 2012, Annual review of immunology.
[5] R. Camerini-Otero,et al. Sensitive mapping of recombination hotspots using sequencing-based detection of ssDNA , 2012, Genome research.
[6] O. Fernandez-Capetillo,et al. Oncogenic stress sensitizes murine cancers to hypomorphic suppression of ATR. , 2012, The Journal of clinical investigation.
[7] L. Symington,et al. Double-strand break end resection and repair pathway choice. , 2011, Annual review of genetics.
[8] Michel C. Nussenzweig,et al. Translocation-Capture Sequencing Reveals the Extent and Nature of Chromosomal Rearrangements in B Lymphocytes , 2011, Cell.
[9] Stefano Monti,et al. Genome-wide Translocation Sequencing Reveals Mechanisms of Chromosome Breaks and Rearrangements in B Cells , 2011, Cell.
[10] M. Nussenzweig,et al. Regulation of DNA end joining, resection, and immunoglobulin class switch recombination by 53BP1. , 2011, Molecular cell.
[11] F. Alt,et al. Mechanisms that promote and suppress chromosomal translocations in lymphocytes. , 2011, Annual review of immunology.
[12] P. Reaper,et al. Discovery of potent and selective inhibitors of ataxia telangiectasia mutated and Rad3 related (ATR) protein kinase as potential anticancer agents. , 2011, Journal of medicinal chemistry.
[13] F. Alt,et al. The RNA Exosome Targets the AID Cytidine Deaminase to Both Strands of Transcribed Duplex DNA Substrates , 2011, Cell.
[14] B. Helmink,et al. H2AX Prevents CtIP-Mediated DNA End Resection and Aberrant Repair in G1-Phase Lymphocytes , 2010, Nature.
[15] M. Nussenzweig,et al. Deep-sequencing identification of the genomic targets of the cytidine deaminase AID and its cofactor RPA in B lymphocytes , 2011, Nature Immunology.
[16] D. Schatz,et al. Uracil residues dependent on the deaminase AID in immunoglobulin gene variable and switch regions , 2011, Nature Immunology.
[17] Vasco M. Barreto,et al. Activation-Induced Cytidine Deaminase Targets DNA at Sites of RNA Polymerase II Stalling by Interaction with Spt5 , 2010, Cell.
[18] M. Kastan,et al. Multiple roles of ATM in monitoring and maintaining DNA integrity , 2010, FEBS letters.
[19] G. Oakley,et al. Replication protein A: directing traffic at the intersection of replication and repair. , 2010, Frontiers in bioscience.
[20] David G. Schatz,et al. The In Vivo Pattern of Binding of RAG1 and RAG2 to Antigen Receptor Loci , 2010, Cell.
[21] Jeremy M. Stark,et al. 53BP1 Inhibits Homologous Recombination in Brca1-Deficient Cells by Blocking Resection of DNA Breaks , 2010, Cell.
[22] M. Nussenzweig,et al. 53BP1 regulates DNA resection and the choice between classical and alternative end joining during class switch recombination , 2010, The Journal of experimental medicine.
[23] Michael S. Becker,et al. The role of mechanistic factors in promoting chromosomal translocations found in lymphoid and other cancers. , 2010, Advances in immunology.
[24] Thomas Ried,et al. AID produces DNA double-strand breaks in non-Ig genes and mature B cell lymphomas with reciprocal chromosome translocations. , 2009, Molecular cell.
[25] Thomas M. Keane,et al. A simple method for directional transcriptome sequencing using Illumina technology , 2009, Nucleic acids research.
[26] A. Khamlichi,et al. S region sequence, RNA polymerase II, and histone modifications create chromatin accessibility during class switch recombination , 2009, The Journal of experimental medicine.
[27] A. Khamlichi,et al. Immunoglobulin switch μ sequence causes RNA polymerase II accumulation and reduces dA hypermutation , 2009, The Journal of experimental medicine.
[28] J. Chaudhuri,et al. Specific recruitment of protein kinase A to the immunoglobulin locus regulates class-switch recombination , 2009, Nature Immunology.
[29] L. Zou,et al. Single-stranded DNA orchestrates an ATM-to-ATR switch at DNA breaks. , 2009, Molecular cell.
[30] M. Nussenzweig,et al. AID Is Required for the Chromosomal Breaks in c-myc that Lead to c-myc/IgH Translocations , 2008, Cell.
[31] M. Nussenzweig,et al. 53BP1 facilitates long-range DNA end-joining during V(D)J recombination , 2008, Nature.
[32] Eleni P. Mimitou,et al. Sae2, Exo1 and Sgs1 collaborate in DNA double-strand break processing , 2008, Nature.
[33] Sang Eun Lee,et al. Sgs1 Helicase and Two Nucleases Dna2 and Exo1 Resect DNA Double-Strand Break Ends , 2008, Cell.
[34] D. Lydall,et al. Checkpoint-dependent phosphorylation of Exo1 modulates the DNA damage response , 2008, The EMBO journal.
[35] P. Sung,et al. Mechanism of eukaryotic homologous recombination. , 2008, Annual review of biochemistry.
[36] C. E. Schrader,et al. Mechanism and regulation of class switch recombination. , 2008, Annual review of immunology.
[37] D. Schatz,et al. Two levels of protection for the B cell genome during somatic hypermutation , 2008, Nature.
[38] E. Selsing,et al. Activation-induced cytidine deaminase-dependent DNA breaks in class switch recombination occur during G1 phase of the cell cycle and depend upon mismatch repair. , 2008, The Journal of Immunology.
[39] M. Nussenzweig,et al. ATM Prevents the Persistence and Propagation of Chromosome Breaks in Lymphocytes , 2007, Cell.
[40] 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.
[41] T. Pandita,et al. ATM stabilizes DNA double-strand-break complexes during V(D)J recombination , 2006, Nature.
[42] David Jung,et al. Mechanism and control of V(D)J recombination at the immunoglobulin heavy chain locus. , 2006, Annual review of immunology.
[43] Jiri Bartek,et al. ATM- and cell cycle-dependent regulation of ATR in response to DNA double-strand breaks , 2006, Nature Cell Biology.
[44] 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.
[45] F. Alt,et al. Replication protein A interacts with AID to promote deamination of somatic hypermutation targets , 2004, Nature.
[46] F. Alt,et al. The role of the non‐homologous end‐joining pathway in lymphocyte development , 2004, Immunological reviews.
[47] Samuel H. Wilson,et al. Increased postischemic brain injury in mice deficient in uracil-DNA glycosylase. , 2004, The Journal of clinical investigation.
[48] P. Modrich,et al. Mechanism of 5'-directed excision in human mismatch repair. , 2003, Molecular cell.
[49] F. Alt,et al. Histone H2AX A Dosage-Dependent Suppressor of Oncogenic Translocations and Tumors , 2003, Cell.
[50] M. Nussenzweig,et al. H2AX Is Required for Recombination Between Immunoglobulin Switch Regions but Not for Intra-Switch Region Recombination or Somatic Hypermutation , 2003, The Journal of experimental medicine.
[51] Stephen J. Elledge,et al. Sensing DNA Damage Through ATRIP Recognition of RPA-ssDNA Complexes , 2003, Science.
[52] Junjie Chen,et al. p53 Binding Protein 53BP1 Is Required for DNA Damage Responses and Tumor Suppression in Mice , 2003, Molecular and Cellular Biology.
[53] D. Baltimore,et al. Essential and dispensable roles of ATR in cell cycle arrest and genome maintenance. , 2003, Genes & development.
[54] M. Kastan,et al. DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation , 2003, Nature.
[55] F. Alt,et al. Internal IgH class switch region deletions are position-independent and enhanced by AID expression , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[56] R. Bambara,et al. Mechanism Underlying Replication Protein A Stimulation of DNA Ligase I* , 2002, The Journal of Biological Chemistry.
[57] T. Honjo,et al. Molecular mechanism of class switch recombination: linkage with somatic hypermutation. , 2002, Annual review of immunology.
[58] Thomas Ried,et al. AID is required to initiate Nbs1/γ-H2AX focus formation and mutations at sites of class switching , 2001, Nature.
[59] Riccardo Dalla-Favera,et al. Mechanisms of chromosomal translocations in B cell lymphomas , 2001, Oncogene.
[60] J. Haber,et al. Regulation of Saccharomyces Rad53 checkpoint kinase during adaptation from DNA damage-induced G2/M arrest. , 2001, Molecular cell.
[61] Thomas Ried,et al. Response to RAG-mediated V(D)J cleavage by NBS1 and γ-H2AX , 2000 .
[62] T. Honjo,et al. Class Switch Recombination and Hypermutation Require Activation-Induced Cytidine Deaminase (AID), a Potential RNA Editing Enzyme , 2000, Cell.
[63] D. Schatz,et al. The RAG proteins and V(D)J recombination: complexes, ends, and transposition. , 2000, Annual review of immunology.
[64] T. Ried,et al. Response to RAG-mediated VDJ cleavage by NBS1 and gamma-H2AX. , 2000, Science.
[65] E. Rogakou,et al. Megabase Chromatin Domains Involved in DNA Double-Strand Breaks in Vivo , 1999, The Journal of cell biology.
[66] R. Bambara,et al. Replication Protein A Stimulates Long Patch DNA Base Excision Repair* , 1998, The Journal of Biological Chemistry.
[67] L. Pasqualucci,et al. BCL-6 mutations in normal germinal center B cells: evidence of somatic hypermutation acting outside Ig loci. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[68] U. Storb,et al. Mutation of BCL-6 gene in normal B cells by the process of somatic hypermutation of Ig genes. , 1998, Science.
[69] F. Alt,et al. Deletion of the IgH intronic enhancer and associated matrix-attachment regions decreases, but does not abolish, class switching at the mu locus. , 1998, International immunology.
[70] S. Kowalczykowski,et al. Rad52 protein stimulates DNA strand exchange by Rad51 and replication protein A , 1998, Nature.
[71] Y. L. Lin,et al. The Evolutionarily Conserved Zinc Finger Motif in the Largest Subunit of Human Replication Protein A Is Required for DNA Replication and Mismatch Repair but Not for Nucleotide Excision Repair* , 1998, The Journal of Biological Chemistry.
[72] U. Storb,et al. Somatic hypermutation of immunoglobulin genes is linked to transcription. , 1998, Current topics in microbiology and immunology.
[73] M. Wold. Replication protein A: a heterotrimeric, single-stranded DNA-binding protein required for eukaryotic DNA metabolism. , 1997, Annual review of biochemistry.
[74] Francis Collins,et al. Atm-Deficient Mice: A Paradigm of Ataxia Telangiectasia , 1996, Cell.
[75] U. Storb,et al. Somatic hypermutation of immunoglobulin genes is linked to transcription initiation. , 1996, Immunity.
[76] H. Griesser,et al. MSH2 deficient mice are viable and susceptible to lymphoid tumours , 1995, Nature Genetics.
[77] P. Sung,et al. DNA strand exchange mediated by a RAD51-ssDNA nucleoprotein filament with polarity opposite to that of RecA , 1995, Cell.
[78] J. Haber,et al. DNA structure-dependent requirements for yeast RAD genes in gene conversion , 1995, Nature.
[79] K. Rajewsky,et al. Independent control of immunoglobulin switch recombination at individual switch regions evidenced through Cre-loxP-mediated gene targeting , 1993, Cell.
[80] E. Egelman,et al. Similarity of the yeast RAD51 filament to the bacterial RecA filament. , 1993, Science.
[81] N. Kleckner,et al. DMC1: A meiosis-specific yeast homolog of E. coli recA required for recombination, synaptonemal complex formation, and cell cycle progression , 1992, Cell.
[82] U. Krawinkel,et al. Directed Ig class switch recombination in activated murine B cells. , 1987, The EMBO journal.
[83] M. Hummel,et al. Switch region content of hybridomas: the two spleen cell Igh loci tend to rearrange to the same isotype. , 1987, Journal of immunology.