The concerted roles of FANCM and Rad52 in the protection of common fragile sites
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Lei Li | Shibo Li | Hailong Wang | Xiaohua Wu | J. Oaks | Jianping Ren
[1] Jiadong Wang,et al. BRCA2 antagonizes classical and alternative nonhomologous end-joining to prevent gross genomic instability , 2017, Nature Communications.
[2] F. Jessen,et al. Association Between Loss-of-Function Mutations Within the FANCM Gene and Early-Onset Familial Breast Cancer , 2017, JAMA oncology.
[3] Sofia Khan,et al. FANCM mutation c.5791C>T is a risk factor for triple-negative breast cancer in the Finnish population , 2017, Breast Cancer Research and Treatment.
[4] F. Storici,et al. Rad52 Inverse Strand Exchange Drives RNA-Templated DNA Double-Strand Break Repair. , 2017, Molecular cell.
[5] Lara E Sucheston-Campbell,et al. Germline whole exome sequencing and large-scale replication identifies FANCM as a likely high grade serous ovarian cancer susceptibility gene , 2017, Oncotarget.
[6] J. Lukas,et al. Mammalian RAD52 Functions in Break-Induced Replication Repair of Collapsed DNA Replication Forks , 2016, Molecular cell.
[7] I. Hickson,et al. RAD52 Facilitates Mitotic DNA Synthesis Following Replication Stress. , 2016, Molecular cell.
[8] C. Schildkraut,et al. FANCD2 Facilitates Replication through Common Fragile Sites. , 2016, Molecular cell.
[9] Jeremy M. Stark,et al. Regulation of Single-Strand Annealing and its Role in Genome Maintenance. , 2016, Trends in genetics : TIG.
[10] B. Kerem,et al. The complex nature of fragile site plasticity and its importance in cancer. , 2016, Current opinion in cell biology.
[11] A. D’Andrea,et al. The Fanconi anaemia pathway: new players and new functions , 2016, Nature Reviews Molecular Cell Biology.
[12] P. Sung,et al. Functions and regulation of the multitasking FANCM family of DNA motor proteins , 2015, Genes & development.
[13] B. Kerem,et al. Oncogenes create a unique landscape of fragile sites , 2015, Nature Communications.
[14] M. Jasin,et al. Homologous recombination and human health: the roles of BRCA1, BRCA2, and associated proteins. , 2015, Cold Spring Harbor perspectives in biology.
[15] Rodney Rothstein,et al. Mechanisms and Regulation of Mitotic Recombination in Saccharomyces cerevisiae , 2014, Genetics.
[16] F. Couch,et al. Exome sequencing identifies FANCM as a susceptibility gene for triple-negative breast cancer , 2014, Proceedings of the National Academy of Sciences.
[17] Jing He,et al. CtIP maintains stability at common fragile sites and inverted repeats by end resection-independent endonuclease activity. , 2014, Molecular cell.
[18] Lei Li,et al. Structure analysis of FAAP24 reveals single-stranded DNA-binding activity and domain functions in DNA damage response , 2013, Cell Research.
[19] S. Powell,et al. RAD52 inactivation is synthetically lethal with deficiencies in BRCA1 and PALB2 in addition to BRCA2 through RAD51-mediated homologous recombination , 2013, Oncogene.
[20] Lei Li,et al. FANCM and FAAP24 maintain genome stability via cooperative as well as unique functions. , 2013, Molecular cell.
[21] S. Powell,et al. Rad51 Paralog Complexes BCDX2 and CX3 Act at Different Stages in the BRCA1-BRCA2-Dependent Homologous Recombination Pathway , 2012, Molecular and Cellular Biology.
[22] B. Kerem,et al. The complex basis underlying common fragile site instability in cancer. , 2012, Trends in genetics : TIG.
[23] Linda Z. Shi,et al. CtIP Protein Dimerization Is Critical for Its Recruitment to Chromosomal DNA Double-stranded Breaks* , 2012, The Journal of Biological Chemistry.
[24] B. Kerem,et al. Failure of origin activation in response to fork stalling leads to chromosomal instability at fragile sites. , 2011, Molecular cell.
[25] M. Jasin,et al. Homology-directed Fanconi anemia pathway crosslink repair is dependent on DNA replication , 2011, Nature structural & molecular biology.
[26] W. Heyer,et al. Who's who in human recombination: BRCA2 and RAD52 , 2010, Proceedings of the National Academy of Sciences.
[27] T. Pandita,et al. Rad52 inactivation is synthetically lethal with BRCA2 deficiency , 2010, Proceedings of the National Academy of Sciences.
[28] S. Kowalczykowski,et al. Purified human BRCA2 stimulates RAD51-mediated recombination , 2010, Nature.
[29] A. D’Andrea,et al. The FANCM/FAAP24 complex is required for the DNA interstrand crosslink-induced checkpoint response. , 2010, Molecular cell.
[30] P. Sung,et al. MHF1-MHF2, a histone-fold-containing protein complex, participates in the Fanconi anemia pathway via FANCM. , 2010, Molecular cell.
[31] Weidong Wang,et al. A histone-fold complex and FANCM form a conserved DNA-remodeling complex to maintain genome stability. , 2010, Molecular cell.
[32] R. Schwab,et al. ATR activation and replication fork restart are defective in FANCM‐deficient cells , 2010, The EMBO journal.
[33] K. Mrasek,et al. New aspects on chromosomal instability: chromosomal break-points in Fanconi anemia patients co-localize on the molecular level with fragile sites. , 2009, International journal of oncology.
[34] S. West,et al. FANCM connects the genome instability disorders Bloom's Syndrome and Fanconi Anemia. , 2009, Molecular cell.
[35] K. Eckert,et al. DNA structure and the Werner protein modulate human DNA polymerase delta-dependent replication dynamics within the common fragile site FRA16D , 2009, Nucleic acids research.
[36] H. Joenje,et al. Fancm-deficient mice reveal unique features of Fanconi anemia complementation group M. , 2009, Human molecular genetics.
[37] Bing Xia,et al. Recruitment of fanconi anemia and breast cancer proteins to DNA damage sites is differentially governed by replication. , 2009, Molecular cell.
[38] R. Rothstein,et al. Rad52 , 2009, Current Biology.
[39] I. Hickson,et al. Replication stress induces sister-chromatid bridging at fragile site loci in mitosis , 2009, Nature Cell Biology.
[40] S. Elledge,et al. FANCM and FAAP24 function in ATR-mediated checkpoint signaling independently of the Fanconi anemia core complex. , 2008, Molecular cell.
[41] A. Constantinou,et al. Remodeling of DNA replication structures by the branch point translocase FANCM , 2008, Proceedings of the National Academy of Sciences.
[42] Weidong Wang,et al. FANCM of the Fanconi anemia core complex is required for both monoubiquitination and DNA repair. , 2008, Human molecular genetics.
[43] A. Papavassiliou,et al. Oncogene-induced replication stress preferentially targets common fragile sites in preneoplastic lesions. A genome-wide study , 2008, Oncogene.
[44] A. Gurtan,et al. Cell cycle-dependent chromatin loading of the Fanconi anemia core complex by FANCM/FAAP24. , 2008, Blood.
[45] Xiaohua Wu,et al. Cell Cycle-dependent Complex Formation of BRCA1·CtIP·MRN Is Important for DNA Double-strand Break Repair* , 2008, Journal of Biological Chemistry.
[46] Andrzej Stasiak,et al. The Fanconi anemia protein FANCM can promote branch migration of Holliday junctions and replication forks. , 2008, Molecular cell.
[47] T. Glover,et al. Chromosome fragile sites. , 2007, Annual review of genetics.
[48] Weidong Wang. Emergence of a DNA-damage response network consisting of Fanconi anaemia and BRCA proteins , 2007, Nature Reviews Genetics.
[49] C. Freudenreich,et al. An AT-rich sequence in human common fragile site FRA16D causes fork stalling and chromosome breakage in S. cerevisiae. , 2007, Molecular cell.
[50] Xiaohua Wu,et al. The Mre11 Complex Mediates the S-Phase Checkpoint through an Interaction with Replication Protein A , 2007, Molecular and Cellular Biology.
[51] Bhuvanesh Singh,et al. Downregulation of Fanconi Anemia Genes in Sporadic Head and Neck Squamous Cell Carcinoma , 2007, ORL.
[52] S. West,et al. Identification of FAAP24, a Fanconi anemia core complex protein that interacts with FANCM. , 2007, Molecular cell.
[53] Aaron Bensimon,et al. Oncogene-induced senescence is a DNA damage response triggered by DNA hyper-replication , 2006, Nature.
[54] Dimitris Kletsas,et al. Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints , 2006, Nature.
[55] J. Jonkers,et al. Mouse models of BRCA1 and BRCA2 deficiency: past lessons, current understanding and future prospects , 2006, Oncogene.
[56] T. Glover,et al. Common fragile sites as targets for chromosome rearrangements. , 2006, DNA repair.
[57] Anne E Carpenter,et al. A Lentiviral RNAi Library for Human and Mouse Genes Applied to an Arrayed Viral High-Content Screen , 2006, Cell.
[58] J. Pereira-Leal,et al. The vertebrate Hef ortholog is a component of the Fanconi anemia tumor-suppressor pathway , 2005, Nature Structural &Molecular Biology.
[59] T. Ørntoft,et al. DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis , 2005, Nature.
[60] Dimitris Kletsas,et al. Activation of the DNA damage checkpoint and genomic instability in human precancerous lesions , 2005, Nature.
[61] A. D’Andrea,et al. The Fanconi anemia pathway is required for the DNA replication stress response and for the regulation of common fragile site stability. , 2005, Human molecular genetics.
[62] Zhao-Qi Wang,et al. Human Fanconi anemia monoubiquitination pathway promotes homologous DNA repair. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[63] M. Kastan,et al. BRCA1 Is Required for Common-Fragile-Site Stability via Its G2/M Checkpoint Function , 2004, Molecular and Cellular Biology.
[64] W. Hahn,et al. Telomerase Maintains Telomere Structure in Normal Human Cells , 2003, Cell.
[65] M. Jasin. Homologous repair of DNA damage and tumorigenesis:the BRCA connection , 2002, Oncogene.
[66] T. Glover,et al. ATR Regulates Fragile Site Stability , 2002, Cell.
[67] B. Morolli,et al. Targeted Inactivation of Mouse RAD52Reduces Homologous Recombination but Not Resistance to Ionizing Radiation , 1998, Molecular and Cellular Biology.
[68] S. Scherer,et al. Molecular characterization of a common fragile site (FRA7H) on human chromosome 7 by the cloning of a simian virus 40 integration site. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[69] P. Hasty,et al. A mutation in mouse rad51 results in an early embryonic lethal that is suppressed by a mutation in p53 , 1996, Molecular and cellular biology.
[70] K. Nakao,et al. Targeted disruption of the Rad51 gene leads to lethality in embryonic mice. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[71] T. Glover,et al. FRA3B extends over a broad region and contains a spontaneous HPV16 integration site: direct evidence for the coincidence of viral integration sites and fragile sites. , 1996, Human molecular genetics.
[72] B. Dutrillaux,et al. Common fragile sites: mechanisms of instability revisited. , 2012, Trends in genetics : TIG.
[73] J. Fryns,et al. Human chromosome fragility. , 2008, Biochimica et biophysica acta.
[74] Link,et al. Mouse models of BRCA 1 and BRCA 2 deficiency : past lessons , current understanding and future prospects , 2022 .