Stephen P Jackson

Summary

Affiliation: University of Cambridge
Country: UK

Publications

  1. pmc Human CtIP mediates cell cycle control of DNA end resection and double strand break repair
    Pablo Huertas
    Gurdon Institute and Department of Zoology, University of Cambridge, Cambridge CB2 1QN, United Kingdom
    J Biol Chem 284:9558-65. 2009
  2. pmc Replication stress induces 53BP1-containing OPT domains in G1 cells
    Jeanine A Harrigan
    The Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, England, UK
    J Cell Biol 193:97-108. 2011
  3. pmc Structure-specific DNA endonuclease Mus81/Eme1 generates DNA damage caused by Chk1 inactivation
    Josep V Forment
    The Gurdon Institute and the Department of Biochemistry, University of Cambridge, Cambridge, United Kingdom
    PLoS ONE 6:e23517. 2011
  4. pmc ATM-dependent phosphorylation of heterogeneous nuclear ribonucleoprotein K promotes p53 transcriptional activation in response to DNA damage
    Abdeladim Moumen
    DNA Damage Response Group, Basic Medical Science Department, St George s University of London, London, UK
    Cell Cycle 12:698-704. 2013
  5. pmc CtIP Mutations Cause Seckel and Jawad Syndromes
    Per Qvist
    Department of Human Genetics and Department of Biomedicine, Aarhus University, Aarhus, Denmark
    PLoS Genet 7:e1002310. 2011
  6. ncbi request reprint Regulation of DNA damage responses by ubiquitin and SUMO
    Stephen P Jackson
    The Gurdon Institute and the Department of Biochemistry, University of Cambridge, Cambridge, UK
    Mol Cell 49:795-807. 2013
  7. pmc The DNA-damage response in human biology and disease
    Stephen P Jackson
    The Gurdon Institute and Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
    Nature 461:1071-8. 2009
  8. pmc The DNA-damage response: new molecular insights and new approaches to cancer therapy
    Stephen P Jackson
    Department of Zoology, The Gurdon Institute, University of Cambridge, Cambridge, UK
    Biochem Soc Trans 37:483-94. 2009
  9. ncbi request reprint Conserved modes of recruitment of ATM, ATR and DNA-PKcs to sites of DNA damage
    Jacob Falck
    The Wellcome Trust and Cancer Research UK Gurdon Institute, and Department of Zoology, Cambridge University, Tennis Court Road, Cambridge CB2 1QN, UK
    Nature 434:605-11. 2005
  10. pmc Human CtIP promotes DNA end resection
    Alessandro A Sartori
    The Wellcome Trust and Cancer Research UK Gurdon Institute, and Department of Zoology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
    Nature 450:509-14. 2007

Detail Information

Publications72

  1. pmc Human CtIP mediates cell cycle control of DNA end resection and double strand break repair
    Pablo Huertas
    Gurdon Institute and Department of Zoology, University of Cambridge, Cambridge CB2 1QN, United Kingdom
    J Biol Chem 284:9558-65. 2009
    ..These results suggest that CDK-mediated control of resection in human cells operates by mechanisms similar to those recently established in yeast...
  2. pmc Replication stress induces 53BP1-containing OPT domains in G1 cells
    Jeanine A Harrigan
    The Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, England, UK
    J Cell Biol 193:97-108. 2011
    ..These findings invoke a model wherein incomplete DNA synthesis during S phase leads to a DNA damage response and formation of 53BP1-OPT domains in the subsequent G1...
  3. pmc Structure-specific DNA endonuclease Mus81/Eme1 generates DNA damage caused by Chk1 inactivation
    Josep V Forment
    The Gurdon Institute and the Department of Biochemistry, University of Cambridge, Cambridge, United Kingdom
    PLoS ONE 6:e23517. 2011
    ..Chk1-mediated protection of replication forks from Mus81/Eme1 even under otherwise unchallenged conditions is therefore vital to prevent uncontrolled fork collapse and ensure proper S-phase progression in human cells...
  4. pmc ATM-dependent phosphorylation of heterogeneous nuclear ribonucleoprotein K promotes p53 transcriptional activation in response to DNA damage
    Abdeladim Moumen
    DNA Damage Response Group, Basic Medical Science Department, St George s University of London, London, UK
    Cell Cycle 12:698-704. 2013
    ..These findings thereby establish hnRNP K as an ATM target and help define how ATM orchestrates p53-dependent transcriptional responses in response to genotoxic stress...
  5. pmc CtIP Mutations Cause Seckel and Jawad Syndromes
    Per Qvist
    Department of Human Genetics and Department of Biomedicine, Aarhus University, Aarhus, Denmark
    PLoS Genet 7:e1002310. 2011
    ..This work thus identifies CtIP as a disease gene for Seckel and Jawad syndromes and defines a new type of genetic disease mechanism in which a dominant negative mutation yields a recessively inherited disorder...
  6. ncbi request reprint Regulation of DNA damage responses by ubiquitin and SUMO
    Stephen P Jackson
    The Gurdon Institute and the Department of Biochemistry, University of Cambridge, Cambridge, UK
    Mol Cell 49:795-807. 2013
    ....
  7. pmc The DNA-damage response in human biology and disease
    Stephen P Jackson
    The Gurdon Institute and Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
    Nature 461:1071-8. 2009
    ..Our improving understanding of DNA-damage responses is providing new avenues for disease management...
  8. pmc The DNA-damage response: new molecular insights and new approaches to cancer therapy
    Stephen P Jackson
    Department of Zoology, The Gurdon Institute, University of Cambridge, Cambridge, UK
    Biochem Soc Trans 37:483-94. 2009
    ..Finally, I explain how our increasing knowledge of the DDR is suggesting new avenues for treating cancer and provide an example of a DDR-inhibitory drug that is showing promise in clinical trials...
  9. ncbi request reprint Conserved modes of recruitment of ATM, ATR and DNA-PKcs to sites of DNA damage
    Jacob Falck
    The Wellcome Trust and Cancer Research UK Gurdon Institute, and Department of Zoology, Cambridge University, Tennis Court Road, Cambridge CB2 1QN, UK
    Nature 434:605-11. 2005
    ....
  10. pmc Human CtIP promotes DNA end resection
    Alessandro A Sartori
    The Wellcome Trust and Cancer Research UK Gurdon Institute, and Department of Zoology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
    Nature 450:509-14. 2007
    ..These findings establish evolutionarily conserved roles for CtIP-like proteins in controlling DSB resection, checkpoint signalling and homologous recombination...
  11. pmc Phospho-dependent interactions between NBS1 and MDC1 mediate chromatin retention of the MRN complex at sites of DNA damage
    J Ross Chapman
    Department of Zoology, Wellcome Trust and Cancer Research UK Gurdon Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
    EMBO Rep 9:795-801. 2008
    ..These findings provide a molecular explanation for the MDC1-MRN interaction and yield insights into how MDC1 coordinates the focal assembly and activation of several DDR factors in response to DNA damage...
  12. pmc Regulation of DNA-damage responses and cell-cycle progression by the chromatin remodelling factor CHD4
    Sophie E Polo
    Department of Biochemistry, The Gurdon Institute, University of Cambridge, Cambridge, UK
    EMBO J 29:3130-9. 2010
    ..These results provide new insights into how the chromatin remodelling complex NuRD contributes to maintaining genome stability...
  13. ncbi request reprint ATM- and cell cycle-dependent regulation of ATR in response to DNA double-strand breaks
    Ali Jazayeri
    The Wellcome Trust and Cancer Research UK Gurdon Institute, and Department of Zoology, Cambridge University, Tennis Court Road, Cambridge, CB2 1QN, UK
    Nat Cell Biol 8:37-45. 2006
    ..Thus, in response to DSBs, ATR activation is regulated by ATM in a cell-cycle dependent manner...
  14. pmc CDK targets Sae2 to control DNA-end resection and homologous recombination
    Pablo Huertas
    The Wellcome Trust and Cancer Research UK Gurdon Institute, and Department of Zoology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
    Nature 455:689-92. 2008
    ..These findings therefore provide a mechanistic basis for cell-cycle control of DSB repair and highlight the importance of regulating DSB resection...
  15. pmc The non-homologous end-joining protein Nej1p is a target of the DNA damage checkpoint
    Peter Ahnesorg
    Wellcome Trust and Cancer Research UK Gurdon Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, United Kingdom
    DNA Repair (Amst) 6:190-201. 2007
    ....
  16. ncbi request reprint hnRNP K: an HDM2 target and transcriptional coactivator of p53 in response to DNA damage
    Abdeladim Moumen
    The Wellcome Trust and Cancer Research UK Gurdon Institute and Department of Zoology, Cambridge University, Tennis Court Road, Cambridge CB2 1QN, United Kingdom
    Cell 123:1065-78. 2005
    ..These findings establish hnRNP K as a new HDM2 target and show that, by serving as a cofactor for p53, hnRNP K plays key roles in coordinating transcriptional responses to DNA damage...
  17. pmc CDK targeting of NBS1 promotes DNA-end resection, replication restart and homologous recombination
    Jacob Falck
    Department of Biochemistry, Wellcome Trust and Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge, UK
    EMBO Rep 13:561-8. 2012
    ..Thus, CDK-mediated NBS1 phosphorylation defines a molecular switch that controls the choice of repair mode for DSBs...
  18. pmc Crystal structure of human XLF/Cernunnos reveals unexpected differences from XRCC4 with implications for NHEJ
    Yi Li
    Department of Biochemistry, University of Cambridge, Cambridge, UK
    EMBO J 27:290-300. 2008
    ..Our data are most consistent with head-to-head interactions in a 2:2:1 XRCC4:XLF:Ligase IV complex...
  19. pmc DNA damage signaling in response to double-strand breaks during mitosis
    Simona Giunta
    Wellcome Trust and Cancer Research UK Gurdon Institute, University of Cambridge, CB2 1QN Cambridge, England, UK
    J Cell Biol 190:197-207. 2010
    ..Finally, we present data suggesting that induction of a primary DDR in mitosis is important because transient inactivation of ATM and DNA-PK renders mitotic cells hypersensitive to DSB-inducing agents...
  20. ncbi request reprint Yeast Nhp6A/B and mammalian Hmgb1 facilitate the maintenance of genome stability
    Sabrina Giavara
    The Wellcome Trust and Cancer Research UK Gurdon Institute and Department of Zoology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, United Kingdom
    Curr Biol 15:68-72. 2005
    ..Taken together, these data indicate that Nhp6A/B and Hmgb1 protect DNA from damaging agents and thus guard against the generation of genomic aberrations...
  21. pmc Saccharomyces cerevisiae histone H2A Ser122 facilitates DNA repair
    Anne C Harvey
    Department of Biochemistry, University of Cambridge, UK
    Genetics 170:543-53. 2005
    ....
  22. pmc The Gam protein of bacteriophage Mu is an orthologue of eukaryotic Ku
    Fabrizio d'Adda di Fagagna
    The Wellcome Trust Cancer Research UK Institute of Cancer and Developmental Biology, University of Cambridge, Tennis Court Road, UK
    EMBO Rep 4:47-52. 2003
    ..These data reveal structural and functional parallels between bacteriophage Gam and eukaryotic Ku and suggest that their functions have been evolutionarily conserved...
  23. pmc DNA helicases Sgs1 and BLM promote DNA double-strand break resection
    Serge Gravel
    The Wellcome Trust and Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, United Kingdom
    Genes Dev 22:2767-72. 2008
    ..Collectively, these data establish evolutionarily conserved roles for the BLM and Sgs1 helicases in DSB processing, signaling, and repair...
  24. pmc Human SIRT6 promotes DNA end resection through CtIP deacetylation
    Abderrahmane Kaidi
    Gurdon Institute and Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
    Science 329:1348-53. 2010
    ..These findings further clarify how SIRT6 promotes genome stability...
  25. pmc KAT5 tyrosine phosphorylation couples chromatin sensing to ATM signalling
    Abderrahmane Kaidi
    The Gurdon Institute and Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
    Nature 498:70-4. 2013
    ..These findings define KAT5 tyrosine phosphorylation as a key event in the sensing of genomic and chromatin perturbations, and highlight a key role for c-Abl in such processes...
  26. ncbi request reprint MDC1/NFBD1: a key regulator of the DNA damage response in higher eukaryotes
    Manuel Stucki
    Department of Zoology, The Wellcome Trust Cancer Research UK, Gurdon Institute of Cancer and Developmental Biology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QR, UK
    DNA Repair (Amst) 3:953-7. 2004
    ..Thus, MDC1/NFBD1 appears to be a key regulator of the DNA damage response in mammalian cells...
  27. pmc Mammalian SUMO E3-ligases PIAS1 and PIAS4 promote responses to DNA double-strand breaks
    Yaron Galanty
    The Wellcome Trust and Cancer Research UK Gurdon Institute, and Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
    Nature 462:935-9. 2009
    ..These findings thus identify PIAS1 and PIAS4 as components of the DDR and reveal how protein recruitment to DSB sites is controlled by coordinated SUMOylation and ubiquitylation...
  28. pmc Spreading of mammalian DNA-damage response factors studied by ChIP-chip at damaged telomeres
    Andreas Meier
    The Wellcome Trust and Cancer Research UK Gurdon Institute, Department of Zoology, University of Cambridge, Cambridge, UK
    EMBO J 26:2707-18. 2007
    ..Finally, we observe weak gammaH2AX signals at telomeres of proliferating cells, but not in hTERT immortalised cells, suggesting that low telomerase activity leads to telomere uncapping and senescence in proliferating primary cells...
  29. ncbi request reprint MDC1 is required for the intra-S-phase DNA damage checkpoint
    Michal Goldberg
    The Wellcome Trust Cancer Research UK Institute of Cancer and Developmental Biology and Department of Zoology, University of Cambridge, Cambridge CB2 1QR, UK
    Nature 421:952-6. 2003
    ..These findings reveal that MDC1-mediated focus formation by the MRE11 complex at sites of DNA damage is crucial for the efficient activation of the intra-S-phase checkpoint...
  30. ncbi request reprint Separation-of-function mutants of yeast Ku80 reveal a Yku80p-Sir4p interaction involved in telomeric silencing
    Rajat Roy
    Wellcome Trust Cancer Research UK Institute of Cancer and Developmental Biology, and Deparment of Zoology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QR, UK
    J Biol Chem 279:86-94. 2004
    ..Taken together with other data, these findings indicate that the Yku80p-Sir4p interaction plays a vital role in the assembly of telomeric heterochromatin...
  31. pmc Rad9 BRCT domain interaction with phosphorylated H2AX regulates the G1 checkpoint in budding yeast
    Andrew Hammet
    Wellcome Trust and Cancer Research UK Gurdon Institute and Department of Zoology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
    EMBO Rep 8:851-7. 2007
    ..These findings indicate that constitutive Tudor domain-mediated and damage-specific BRCT domain-phospho-H2A-dependent interactions of Rad9 with chromatin cooperate to establish G1 checkpoint arrest...
  32. ncbi request reprint Rapid PIKK-dependent release of Chk1 from chromatin promotes the DNA-damage checkpoint response
    Veronique A J Smits
    The Wellcome Trust and Cancer Research UK Gurdon Institute, Tennis Court Road, Cambridge CB2 1QN, United Kingdom
    Curr Biol 16:150-9. 2006
    ..Within these pathways, the effector kinase Chk1 plays a central role in mediating cell-cycle arrest in response to DNA damage, and it does so by phosphorylating key cell-cycle regulators...
  33. pmc Give me a break, but not in mitosis: the mitotic DNA damage response marks DNA double-strand breaks with early signaling events
    Simona Giunta
    The Gurdon Institute, University of Cambridge, Cambridge, UK
    Cell Cycle 10:1215-21. 2011
    ..We discuss these and other recent findings and suggest how these novel data collectively contribute to our understanding of mitosis and how cells deal with DNA damage during this crucial cell cycle stage...
  34. ncbi request reprint MDC1 directly binds phosphorylated histone H2AX to regulate cellular responses to DNA double-strand breaks
    Manuel Stucki
    The Wellcome Trust Cancer Research UK Gurdon Institute and Department of Zoology, Cambridge University, Tennis Court Road, Cambridge CB2 1QN, United Kingdom
    Cell 123:1213-26. 2005
    ..Thus, binding of MDC1/NFBD1 to gammaH2AX plays a central role in the mammalian response to DNA damage...
  35. ncbi request reprint Identification and characterization of a novel and specific inhibitor of the ataxia-telangiectasia mutated kinase ATM
    Ian Hickson
    KuDOS Pharmaceuticals Ltd, Cambridge Science Park, Milton Road, Cambridge, UK
    Cancer Res 64:9152-9. 2004
    ..We conclude that KU-55933 is a novel, specific, and potent inhibitor of the ATM kinase...
  36. ncbi request reprint Interfaces between the detection, signaling, and repair of DNA damage
    John Rouse
    The Wellcome Trust Cancer Research UK Institute of Cancer and Developmental Biology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QR, UK
    Science 297:547-51. 2002
    ..In contrast, it is still unclear how primary DNA damage is detected and how this interfaces with signal transduction and DNA repair proteins...
  37. ncbi request reprint The Mre11 complex: at the crossroads of dna repair and checkpoint signalling
    Damien D'Amours
    Wellcome Trust and Cancer Research, UK Institute of Cancer and Developmental Biology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QR, UK
    Nat Rev Mol Cell Biol 3:317-27. 2002
    ..The molecular defect that underlies these phenotypes has long been thought to be related to a DNA repair deficiency. However, recent studies have uncovered functions for the Mre11 complex in checkpoint signalling and DNA replication...
  38. pmc Dma/RNF8 proteins are evolutionarily conserved E3 ubiquitin ligases that target septins
    Richard Chahwan
    The Gurdon Institute, University of Cambridge, Cambridge, UK
    Cell Cycle 12:1000-8. 2013
    ..Together, these findings reveal evolutionary and functional conservation of Dma proteins, and suggest that RNF8 maintains genome stability through independent, yet analogous, nuclear and cytoplasmic ubiquitylation activities...
  39. pmc A phospho-proteomic screen identifies substrates of the checkpoint kinase Chk1
    Melanie Blasius
    The Gurdon Institute and Department of Biochemistry, University of Cambridge, Cambridge CB2 1QN, UK
    Genome Biol 12:R78. 2011
    ..Despite its paramount importance, how Chk1 controls these functions remains unclear, mainly because very few Chk1 substrates have hitherto been identified...
  40. ncbi request reprint Structure of an Xrcc4-DNA ligase IV yeast ortholog complex reveals a novel BRCT interaction mode
    Andrew S Doré
    Department of Biochemistry, University of Cambridge, 80 Tennis Court Road, Cambridge, CB2 1GA, UK
    DNA Repair (Amst) 5:362-8. 2006
    ..The structure reveals a novel mode of protein recognition by a tandem BRCT repeat, and in addition provides a molecular basis for a human LIG4 syndrome clinical condition...
  41. pmc Small-molecule-induced DNA damage identifies alternative DNA structures in human genes
    Raphaël Rodriguez
    Department of Chemistry, University of Cambridge, Cambridge, UK
    Nat Chem Biol 8:301-10. 2012
    ..Our unbiased approach to define genomic sites of action for a drug establishes a framework for discovering functional DNA-drug interactions...
  42. ncbi request reprint p53 prevents the accumulation of double-strand DNA breaks at stalled-replication forks induced by UV in human cells
    Shoshana Squires
    Department of Zoology, University of Cambridge, Cambridge, UK
    Cell Cycle 3:1543-57. 2004
    ..We propose that a major mechanism by which p53 maintains genome stability is the prevention of DSB accumulation at long-lived ssDNA regions in stalled-replication forks...
  43. pmc RNF4, a SUMO-targeted ubiquitin E3 ligase, promotes DNA double-strand break repair
    Yaron Galanty
    The Gurdon Institute, Department of Biochemistry, University of Cambridge, Cambridge, United Kingdom
    Genes Dev 26:1179-95. 2012
    ..RNF4 thus operates as a DSB response factor at the crossroads between the SUMO and ubiquitin systems...
  44. pmc Regulation of DNA-end resection by hnRNPU-like proteins promotes DNA double-strand break signaling and repair
    Sophie E Polo
    The Gurdon Institute, Department of Biochemistry, University of Cambridge, UK
    Mol Cell 45:505-16. 2012
    ..Collectively, these results provide insights into how mammalian cells respond to DSBs...
  45. pmc Screen for DNA-damage-responsive histone modifications identifies H3K9Ac and H3K56Ac in human cells
    Jorrit V Tjeertes
    Gurdon Institute, University of Cambridge, Cambridge, UK
    EMBO J 28:1878-89. 2009
    ..Collectively, our data indicate that though most histone modifications do not change appreciably after genotoxic stress, H3K9Ac and H3K56Ac are reduced in response to DNA damage in human cells...
  46. pmc Human HDAC1 and HDAC2 function in the DNA-damage response to promote DNA nonhomologous end-joining
    Kyle M Miller
    The Gurdon Institute, University of Cambridge, Cambridge, UK
    Nat Struct Mol Biol 17:1144-51. 2010
    ....
  47. pmc Yeast Rtt109 promotes genome stability by acetylating histone H3 on lysine 56
    Robert Driscoll
    Wellcome Trust and Cancer Research U K Gurdon Institute and the Department of Zoology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
    Science 315:649-52. 2007
    ..These data establish Rtt109p as a member of a new class of histone acetyltransferases and show that its actions are critical for cell survival in the presence of DNA damage during S phase...
  48. pmc Saccharomyces cerevisiae Sin3p facilitates DNA double-strand break repair
    Ali Jazayeri
    Wellcome Trust Cancer Research UK Gurdon Institute and Department of Zoology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QR, United Kingdom
    Proc Natl Acad Sci U S A 101:1644-9. 2004
    ..Taken together, these results define a role for the Sin3p/Rpd3p complex in the modulation of DNA repair...
  49. ncbi request reprint Binding of chromatin-modifying activities to phosphorylated histone H2A at DNA damage sites
    Jessica A Downs
    The Wellcome Trust Cancer Research UK Gurdon Institute and Department of Zoology, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QR, United Kingdom
    Mol Cell 16:979-90. 2004
    ..Thus, phosphorylation of H2A at DNA damage sites creates a mark recognized by different chromatin modifiers. This interaction leads to stepwise chromatin reconfiguration, allowing efficient DNA repair...
  50. pmc Genome-wide reprogramming in the mouse germ line entails the base excision repair pathway
    Petra Hajkova
    Wellcome Trust Cancer Research U K Gurdon Institute of Cancer and Developmental Biology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
    Science 329:78-82. 2010
    ..We demonstrate that DNA repair through BER represents a core component of genome-wide DNA demethylation in vivo and provides a mechanistic link to the extensive chromatin remodeling in developing PGCs...
  51. pmc BRCA1-associated exclusion of 53BP1 from DNA damage sites underlies temporal control of DNA repair
    J Ross Chapman
    Wellcome Trust and Cancer Research UK Gurdon Institute and Department of Biochemistry, University of Cambridge, Cambridge CB2 1QN, UK
    J Cell Sci 125:3529-34. 2012
    ..Furthermore, the genomic instability exhibited by BRCA1-deficient cells might result from a failure to efficiently exclude 53BP1 from such regions during S phase...
  52. ncbi request reprint Suppression of homologous recombination by the Saccharomyces cerevisiae linker histone
    Jessica A Downs
    The Wellcome Trust Cancer Research UK Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QR, United Kingdom
    Mol Cell 11:1685-92. 2003
    ..Finally, we show that Hho1p is inhibitory to the recombination-dependent mechanism of telomere maintenance. The role of linker histones in genome stability, aging, and tumorigenesis is discussed...
  53. ncbi request reprint ATM and ATR
    Jane M Bradbury
    The Wellcome Trust Cancer Research UK Institute, Tennis Court Road, Cambridge CB2 1QR, UK
    Curr Biol 13:R468. 2003
  54. ncbi request reprint A means to a DNA end: the many roles of Ku
    Jessica A Downs
    Department of Biochemistry, University of Cambridge, 80 Tennis Court Road, Cambridge CB2 1GA, UK
    Nat Rev Mol Cell Biol 5:367-78. 2004
  55. pmc A high-throughput, flow cytometry-based method to quantify DNA-end resection in mammalian cells
    Josep V Forment
    The Gurdon Institute and Department of Biochemistry, University of Cambridge, CB2 1QN Cambridge, United Kingdom
    Cytometry A 81:922-8. 2012
    ..Here, we present a high-throughput flow-cytometry method that allows the use of RPA staining to measure cell proliferation and DNA-damage repair by HR in an unprecedented, unbiased and quantitative manner...
  56. ncbi request reprint XLF interacts with the XRCC4-DNA ligase IV complex to promote DNA nonhomologous end-joining
    Peter Ahnesorg
    The Gurdon Institute, Cambridge University, UK
    Cell 124:301-13. 2006
    ..XLF thus constitutes a novel core component of the mammalian NHEJ apparatus...
  57. ncbi request reprint Activation of the DNA damage response by telomere attrition: a passage to cellular senescence
    Philip M Reaper
    The Wellcome Trust Cancer Research UK Gurdon Institute, University of Cambridge, UK
    Cell Cycle 3:543-6. 2004
    ..We consider the identities of the key DNA damage response factors involved in senescence and discuss a model for the molecular events occurring in pre-senescent cells that ultimately lead to a permanent cell cycle arrest phenotype...
  58. ncbi request reprint Lcd1p recruits Mec1p to DNA lesions in vitro and in vivo
    John Rouse
    Wellcome Trust and Cancer Research UK, Institute of Cancer and Developmental Biology, University of Cambridge, Cambridge CB2 1QR, United Kingdom
    Mol Cell 9:857-69. 2002
    ..Recruitment of Lcd1p to these lesions is independent of Mec1p and Rad9p/Rad24p. Thus, recruitment of Mec1p to DNA lesions by Lcd1p is crucial for the DNA damage response...
  59. ncbi request reprint Chemical inhibition of NAT10 corrects defects of laminopathic cells
    Delphine Larrieu
    The Wellcome Trust Cancer Research UK CRUK Gurdon Institute and Department of Biochemistry, University of Cambridge, CB2 1QN Cambridge, UK
    Science 344:527-32. 2014
    ..These findings provide insights into how NAT10 affects nuclear architecture and suggest alternative strategies for treating laminopathies and aging. ..
  60. ncbi request reprint Identification of a DNA nonhomologous end-joining complex in bacteria
    Geoffrey R Weller
    Cambridge Institute for Medical Research and Department of Haematology, University of Cambridge, Hills Road, Cambridge CB2 2XY, UK
    Science 297:1686-9. 2002
    ....
  61. ncbi request reprint Histone marks: repairing DNA breaks within the context of chromatin
    Kyle M Miller
    The Gurdon Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, U K
    Biochem Soc Trans 40:370-6. 2012
    ....
  62. pmc Regulation of Rad51 function by phosphorylation
    Sonja Flott
    Department of Biochemistry, Wellcome Trust and Cancer Research UK, Gurdon Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
    EMBO Rep 12:833-9. 2011
    ..These data suggest a model in which Mec1-mediated phosphorylation of Rad51 Ser 192 in response to DNA damage controls Rad51 activity and DNA repair by homologous recombination...
  63. pmc Deubiquitylating enzymes and DNA damage response pathways
    Xavier Jacq
    MISSION Therapeutics Ltd, Babraham Research Campus, Cambridge, CB22 3AT, UK
    Cell Biochem Biophys 67:25-43. 2013
    ..Here, we review key deubiquitylating enzymes (DUBs) involved in DDR pathways, and describe how targeting DUBs may lead to selective therapies to treat cancer patients. ..
  64. doi request reprint Chromothripsis and cancer: causes and consequences of chromosome shattering
    Josep V Forment
    The Gurdon Institute and Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
    Nat Rev Cancer 12:663-70. 2012
    ..We also discuss the potential diagnostic, prognostic and therapeutic implications of chromothripsis in cancer...
  65. ncbi request reprint Regulation of histone H3 lysine 56 acetylation in Schizosaccharomyces pombe
    Blerta Xhemalce
    Unite de la Dynamique du Génome, Institut Pasteur, 25 rue du Dr Roux, 75724, Paris Cedex 15, France
    J Biol Chem 282:15040-7. 2007
    ....
  66. ncbi request reprint The interaction of Alba, a conserved archaeal chromatin protein, with Sir2 and its regulation by acetylation
    Stephen D Bell
    Medical Research Council MRC Cancer Cell Unit, The Hutchison MRC Research Centre, Hills Road, Cambridge, CB2 2QH, UK
    Science 296:148-51. 2002
    ..These data provide a paradigm for how Sir2 family proteins influence transcription and suggest that modulation of chromatin structure by acetylation arose before the divergence of the archaeal and eukaryotic lineages...
  67. pmc Screening the yeast genome for new DNA-repair genes
    Ali Jazayeri
    Wellcome Cancer Research UK Institute of Cancer and Developmental Biology and Department of Zoology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QR, UK
    Genome Biol 3:REVIEWS1009. 2002
    ..The availability of the complete genome sequence of Saccharomyces cerevissiae has greatly facilitated the discovery of new genes important for DNA repair...
  68. pmc A new method for high-resolution imaging of Ku foci to decipher mechanisms of DNA double-strand break repair
    Sébastien Britton
    The Wellcome Trust and Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge, CB2 1QN, England, UK
    J Cell Biol 202:579-95. 2013
    ..Furthermore, we use our method to monitor DNA repair and identify mechanisms of repair pathway choice, and we show its utility in defining cellular sensitivities and resistance mechanisms to anticancer agents. ..
  69. pmc Competing roles of DNA end resection and non-homologous end joining functions in the repair of replication-born double-strand breaks by sister-chromatid recombination
    Sandra Muñoz-Galván
    Centro Andaluz de Biologia Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla CSIC, Av Americo Vespucio s n, 41092 Seville, Spain
    Nucleic Acids Res 41:1669-83. 2013
    ..These results further our understanding of the role of DNA resection in repair of replication-born DSBs revealing unanticipated differences between these events and repair of enzymatically induced DSBs...
  70. pmc Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications
    Sophie E Polo
    The Gurdon Institute, Department of Biochemistry, University of Cambridge, Cambridge CB21QN, United Kingdom
    Genes Dev 25:409-33. 2011
    ..We review these regulatory mechanisms and discuss their biological significance to the DDR...
  71. pmc Suppression of retroviral infection by the RAD52 DNA repair protein
    Alan Lau
    KuDOS Pharmaceuticals Limited, 327 Cambridge Science Park, Cambridge, UK
    EMBO J 23:3421-9. 2004
    ..Instead, the mechanism of attenuation of retroviral infection by RAD52 appears to be based upon competition between the RAD52 protein and active integration complexes for the retroviral cDNA genome...
  72. ncbi request reprint Sensing and repairing DNA double-strand breaks
    Stephen P Jackson
    Wellcome Trust and Cancer Research UK Institute of Cancer and Developmental Biology, Tennis Court Road, Cambridge CB2 1QR, UK
    Carcinogenesis 23:687-96. 2002
    ..An increased knowledge of DSB repair and of other DNA DSB responses may therefore provide opportunities for developing more effective treatments for cancer...