RAD51 separation of function mutation disables replication fork maintenance but preserves DSB repair

[1]  Robert Appleby,et al.  Structural basis for stabilisation of the RAD51 nucleoprotein filament by BRCA2 , 2023, Nature communications.

[2]  D. Cortez,et al.  RAD51 bypasses the CMG helicase to promote replication fork reversal , 2023, Science.

[3]  B. Reina-San-Martin,et al.  Activation of homologous recombination in G1 preserves centromeric integrity , 2021, Nature.

[4]  P. Hasty,et al.  TREX2 Exonuclease Causes Spontaneous Mutations and Stress-Induced Replication Fork Defects in Cells Expressing RAD51K133A , 2020, Cell reports.

[5]  P. Sung,et al.  Single-molecule visualization of human RECQ5 interactions with single-stranded DNA recombination intermediates , 2020, Nucleic acids research.

[6]  V. Gottifredi,et al.  Persistent double strand break accumulation does not precede cell death in an Olaparib-sensitive BRCA-deficient colorectal cancer cell model , 2019, Genetics and molecular biology.

[7]  Kejiao Li,et al.  A Genetic Map of the Response to DNA Damage in Human Cells , 2019, Cell.

[8]  Y. Chan,et al.  Non-enzymatic roles of human RAD51 at stalled replication forks , 2018, Nature Communications.

[9]  Maximilian Haeussler,et al.  CRISPOR: intuitive guide selection for CRISPR/Cas9 genome editing experiments and screens , 2018, Nucleic Acids Res..

[10]  M. Kovács,et al.  Human RAD51 rapidly forms intrinsically dynamic nucleoprotein filaments modulated by nucleotide binding state , 2018, Nucleic acids research.

[11]  V. Costanzo,et al.  Fanconi-Anemia-Associated Mutations Destabilize RAD51 Filaments and Impair Replication Fork Protection. , 2017, Cell reports.

[12]  A. Antoni,et al.  Smarcal1-Mediated Fork Reversal Triggers Mre11-Dependent Degradation of Nascent DNA in the Absence of Brca2 and Stable Rad51 Nucleofilaments , 2017, Molecular cell.

[13]  L. Collinson,et al.  A Polar and Nucleotide-Dependent Mechanism of Action for RAD51 Paralogs in RAD51 Filament Remodeling , 2016, Molecular cell.

[14]  P. Hasty,et al.  Deletion of BRCA2 exon 27 causes defects in response to both stalled and collapsed replication forks. , 2014, Mutation research.

[15]  A. Carr,et al.  Replication stress-induced genome instability: the dark side of replication maintenance by homologous recombination. , 2013, Journal of molecular biology.

[16]  P. Hasty,et al.  Two Replication Fork Maintenance Pathways Fuse Inverted Repeats to Rearrange Chromosomes , 2013, Nature.

[17]  A. Carr,et al.  Recombination-restarted replication makes inverted chromosome fusions at inverted repeats , 2012, Nature.

[18]  Hong Wu,et al.  A distinct replication fork protection pathway connects Fanconi anemia tumor suppressors to RAD51-BRCA1/2. , 2012, Cancer cell.

[19]  P. Hasty,et al.  RAD51 Mutants Cause Replication Defects and Chromosomal Instability , 2012, Molecular and Cellular Biology.

[20]  Kevin W Eliceiri,et al.  NIH Image to ImageJ: 25 years of image analysis , 2012, Nature Methods.

[21]  D. Cortez,et al.  Analysis of protein dynamics at active, stalled, and collapsed replication forks. , 2011, Genes & development.

[22]  S. Kowalczykowski,et al.  Two classes of BRC repeats in BRCA2 promote RAD51 nucleoprotein filament function by distinct mechanisms , 2011, Proceedings of the National Academy of Sciences.

[23]  T. Helleday,et al.  Pathways of mammalian replication fork restart , 2010, Nature Reviews Molecular Cell Biology.

[24]  T. Helleday,et al.  Chk1 promotes replication fork progression by controlling replication initiation , 2010, Proceedings of the National Academy of Sciences.

[25]  S. Kowalczykowski,et al.  Purified human BRCA2 stimulates RAD51-mediated recombination , 2010, Nature.

[26]  T. Helleday,et al.  Hydroxyurea-Stalled Replication Forks Become Progressively Inactivated and Require Two Different RAD51-Mediated Pathways for Restart and Repair , 2010, Molecular cell.

[27]  A. Carr,et al.  Nearby inverted repeats fuse to generate acentric and dicentric palindromic chromosomes by a replication template exchange mechanism. , 2009, Genes & development.

[28]  Ashok R. Venkitaraman,et al.  Two modules in the BRC repeats of BRCA2 mediate structural and functional interactions with the RAD51 recombinase , 2009, Nucleic acids research.

[29]  Jeremy M. Stark,et al.  Limiting the Persistence of a Chromosome Break Diminishes Its Mutagenic Potential , 2009, PLoS genetics.

[30]  T. Lohman,et al.  Srs2 disassembles Rad51 filaments by a protein-protein interaction triggering ATP turnover and dissociation of Rad51 from DNA. , 2009, Molecular cell.

[31]  Y. Choi,et al.  High‐throughput knock‐in coupling gene targeting with the HPRT minigene and Cre‐mediated recombination , 2008, Genesis.

[32]  Jeremy M. Stark,et al.  Alternative-NHEJ Is a Mechanistically Distinct Pathway of Mammalian Chromosome Break Repair , 2008, PLoS genetics.

[33]  H. Vogel,et al.  Deletion of Ku80 causes early aging independent of chronic inflammation and Rag-1-induced DSBs , 2007, Mechanisms of Ageing and Development.

[34]  Weidong Wang Emergence of a DNA-damage response network consisting of Fanconi anaemia and BRCA proteins , 2007, Nature Reviews Genetics.

[35]  Edward H Egelman,et al.  Stabilization of RAD51 nucleoprotein filaments by the C-terminal region of BRCA2 , 2007, Nature Structural &Molecular Biology.

[36]  Luca Pellegrini,et al.  A region of human BRCA2 containing multiple BRC repeats promotes RAD51-mediated strand exchange , 2006, Nucleic acids research.

[37]  Michael G. Sehorn,et al.  Recombination Mediator and Rad51 Targeting Activities of a Human BRCA2 Polypeptide* , 2006, Journal of Biological Chemistry.

[38]  J. Thacker The RAD51 gene family, genetic instability and cancer. , 2005, Cancer letters.

[39]  P. Hasty,et al.  A genotoxic screen: rapid analysis of cellular dose-response to a wide range of agents that either damage DNA or alter genome maintenance pathways. , 2004, Mutation research.

[40]  G. Almouzni,et al.  Mouse centric and pericentric satellite repeats form distinct functional heterochromatin , 2004, The Journal of cell biology.

[41]  M. King,et al.  Breast and Ovarian Cancer Risks Due to Inherited Mutations in BRCA1 and BRCA2 , 2003, Science.

[42]  Jeremy M. Stark,et al.  ATP Hydrolysis by Mammalian RAD51 Has a Key Role during Homology-directed DNA Repair* , 2002, The Journal of Biological Chemistry.

[43]  M. Jasin,et al.  BRCA2 is required for homology-directed repair of chromosomal breaks. , 2001, Molecular cell.

[44]  J. Damborský,et al.  Molecular Dissection of Interactions between Rad51 and Members of the Recombination-Repair Group , 2001, Molecular and Cellular Biology.

[45]  Phang-lang Chen,et al.  Expression of BRC Repeats in Breast Cancer Cells Disrupts the BRCA2-Rad51 Complex and Leads to Radiation Hypersensitivity and Loss of G2/M Checkpoint Control* , 1999, The Journal of Biological Chemistry.

[46]  P. Hasty,et al.  Cells deleted for Brca2 COOH terminus exhibit hypersensitivity to gamma-radiation and premature senescence. , 1998, Cancer research.

[47]  Y. Chen,et al.  The BRC repeats in BRCA2 are critical for RAD51 binding and resistance to methyl methanesulfonate treatment. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[48]  G. Eichele,et al.  Embryonic lethality and radiation hypersensitivity mediated by Rad51 in mice lacking Brca2 , 1997, Nature.

[49]  E. Craig,et al.  Genomic libraries and a host strain designed for highly efficient two-hybrid selection in yeast. , 1996, Genetics.

[50]  M. Marinus,et al.  DNA methylation alters the pattern of spontaneous mutation in Escherichia coli cells (mutD) defective in DNA polymerase III proofreading. , 1991, Mutation research.

[51]  A. Bradley,et al.  Target frequency and integration pattern for insertion and replacement vectors in embryonic stem cells , 1991, Molecular and cellular biology.

[52]  E. Friedberg,et al.  DNA Repair and Mutagenesis , 2006 .

[53]  L. Liu,et al.  Tumor cell death induced by topoisomerase-targeting drugs. , 2001, Annual review of pharmacology and toxicology.