Grant S Stewart

Summary

Affiliation: University of Birmingham
Country: UK

Publications

  1. ncbi request reprint MDC1 is a mediator of the mammalian DNA damage checkpoint
    Grant S Stewart
    Verna and Mars McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, Texas 77030, USA
    Nature 421:961-6. 2003
  2. ncbi request reprint Ataxia telangiectasia mutated-deficient B-cell chronic lymphocytic leukemia occurs in pregerminal center cells and results in defective damage response and unrepaired chromosome damage
    Tatjana Stankovic
    University of Birmingham, CRC Institute for Cancer Studies, The Medical School, Edgbaston, United Kingdom
    Blood 99:300-9. 2002
  3. pmc Variations in ATM protein expression during normal lymphoid differentiation and among B-cell-derived neoplasias
    Jane Starczynski
    Department of Histopathology, Birmingham Heartland s Hospital, Birmingham, United Kingdom
    Am J Pathol 163:423-32. 2003
  4. ncbi request reprint Microarray analysis reveals that TP53- and ATM-mutant B-CLLs share a defect in activating proapoptotic responses after DNA damage but are distinguished by major differences in activating prosurvival responses
    Tatjana Stankovic
    Cancer Research UK Institute for Cancer Studies, University of Birmingham, Edgbaston, Birmingham, United Kingdom
    Blood 103:291-300. 2004
  5. doi request reprint The RIDDLE syndrome protein mediates a ubiquitin-dependent signaling cascade at sites of DNA damage
    Grant S Stewart
    Cancer Research UK, Institute for Cancer Studies, University of Birmingham, Edgbaston, Birmingham, UK
    Cell 136:420-34. 2009
  6. ncbi request reprint Solving the RIDDLE of 53BP1 recruitment to sites of damage
    Grant S Stewart
    Cancer Research UK Institute for Cancer Studies, University of Birmingham, Edgbaston, Birmingham, UK
    Cell Cycle 8:1532-8. 2009
  7. pmc RIDDLE immunodeficiency syndrome is linked to defects in 53BP1-mediated DNA damage signaling
    Grant S Stewart
    Cancer Research UK, Institute for Cancer Studies, Birmingham University, Vincent Drive, Edgbaston, Birmingham, United Kingdom
    Proc Natl Acad Sci U S A 104:16910-5. 2007
  8. pmc Mediator of DNA damage checkpoint 1 (MDC1) regulates mitotic progression
    Kelly Townsend
    Cancer Research United Kingdom Institute for Cancer Sciences, University of Birmingham Medical School, Edgbaston, Birmingham B15 2TT, United Kingdom
    J Biol Chem 284:33939-48. 2009
  9. pmc Adenovirus 12 E4orf6 inhibits ATR activation by promoting TOPBP1 degradation
    Andrew N Blackford
    School of Cancer Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TT, United Kingdom
    Proc Natl Acad Sci U S A 107:12251-6. 2010
  10. pmc Serotype-specific inactivation of the cellular DNA damage response during adenovirus infection
    Natalie A Forrester
    University of Birmingham, Birmingham B15 2TT, UK
    J Virol 85:2201-11. 2011

Collaborators

Detail Information

Publications24

  1. ncbi request reprint MDC1 is a mediator of the mammalian DNA damage checkpoint
    Grant S Stewart
    Verna and Mars McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, Texas 77030, USA
    Nature 421:961-6. 2003
    ..These results highlight a crucial role for MDC1 in mediating transduction of the DNA damage signal...
  2. ncbi request reprint Ataxia telangiectasia mutated-deficient B-cell chronic lymphocytic leukemia occurs in pregerminal center cells and results in defective damage response and unrepaired chromosome damage
    Tatjana Stankovic
    University of Birmingham, CRC Institute for Cancer Studies, The Medical School, Edgbaston, United Kingdom
    Blood 99:300-9. 2002
    ....
  3. pmc Variations in ATM protein expression during normal lymphoid differentiation and among B-cell-derived neoplasias
    Jane Starczynski
    Department of Histopathology, Birmingham Heartland s Hospital, Birmingham, United Kingdom
    Am J Pathol 163:423-32. 2003
    ..As a result, immunostaining to identify lymphoid neoplasias with ATM inactivation might only be feasible for tumors derived from the stages where ATM is constitutively highly expressed...
  4. ncbi request reprint Microarray analysis reveals that TP53- and ATM-mutant B-CLLs share a defect in activating proapoptotic responses after DNA damage but are distinguished by major differences in activating prosurvival responses
    Tatjana Stankovic
    Cancer Research UK Institute for Cancer Studies, University of Birmingham, Edgbaston, Birmingham, United Kingdom
    Blood 103:291-300. 2004
    ..Therefore, damage-induced transcriptional fingerprinting can be used to stratify tumors according to their biologic differences and simultaneously identify potential targets for treating refractory tumors...
  5. doi request reprint The RIDDLE syndrome protein mediates a ubiquitin-dependent signaling cascade at sites of DNA damage
    Grant S Stewart
    Cancer Research UK, Institute for Cancer Studies, University of Birmingham, Edgbaston, Birmingham, UK
    Cell 136:420-34. 2009
    ..These RNF168-dependent chromatin modifications orchestrate the accumulation of 53BP1 and BRCA1 to DNA lesions, and their loss is the likely cause of the cellular and developmental phenotypes associated with RIDDLE syndrome...
  6. ncbi request reprint Solving the RIDDLE of 53BP1 recruitment to sites of damage
    Grant S Stewart
    Cancer Research UK Institute for Cancer Studies, University of Birmingham, Edgbaston, Birmingham, UK
    Cell Cycle 8:1532-8. 2009
    ....
  7. pmc RIDDLE immunodeficiency syndrome is linked to defects in 53BP1-mediated DNA damage signaling
    Grant S Stewart
    Cancer Research UK, Institute for Cancer Studies, Birmingham University, Vincent Drive, Edgbaston, Birmingham, United Kingdom
    Proc Natl Acad Sci U S A 104:16910-5. 2007
    ..Therefore, these data indicate the existence of a DNA double-strand break-repair protein that functions upstream of 53BP1 and contributes to the normal development of the human immune system...
  8. pmc Mediator of DNA damage checkpoint 1 (MDC1) regulates mitotic progression
    Kelly Townsend
    Cancer Research United Kingdom Institute for Cancer Sciences, University of Birmingham Medical School, Edgbaston, Birmingham B15 2TT, United Kingdom
    J Biol Chem 284:33939-48. 2009
    ..We suggest therefore that hMDC1 functionally regulates the normal metaphase-to-anaphase transition by modulating the Cdc20-dependent activation of the APC/C...
  9. pmc Adenovirus 12 E4orf6 inhibits ATR activation by promoting TOPBP1 degradation
    Andrew N Blackford
    School of Cancer Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TT, United Kingdom
    Proc Natl Acad Sci U S A 107:12251-6. 2010
    ..Taken together, these data provide insights into how Ad modulates ATR signaling pathways during infection...
  10. pmc Serotype-specific inactivation of the cellular DNA damage response during adenovirus infection
    Natalie A Forrester
    University of Birmingham, Birmingham B15 2TT, UK
    J Virol 85:2201-11. 2011
    ..We suggest that group B and D adenoviruses have evolved mechanisms based on the loss of DNA ligase IV and perhaps other unknown molecules to disable the host cell DNA damage response to promote viral replication...
  11. pmc Adenovirus E4orf3 targets transcriptional intermediary factor 1γ for proteasome-dependent degradation during infection
    Natalie A Forrester
    School of Cancer Sciences, University of Birmingham, Edgbaston, Birmingham, UnitedKingdom
    J Virol 86:3167-79. 2012
    ..Taken together, these studies have identified novel adenovirus targets and have established a new role for the E4orf3 protein during infection...
  12. pmc A role for E1B-AP5 in ATR signaling pathways during adenovirus infection
    Andrew N Blackford
    CR UK Institute for Cancer Studies, The Medical School, The University of Birmingham, Edgbaston, Birmingham B15 2TT, United Kingdom
    J Virol 82:7640-52. 2008
    ..This might have broader implications for the regulation of ATR activity during cellular DNA replication or in response to DNA damage...
  13. doi request reprint A nervous predisposition to unrepaired DNA double strand breaks
    John J Reynolds
    School of Cancer Sciences, College of Medicine and Dentistry, University of Birmingham, IBR West Extension, First Floor, Vincent Drive, Edgbaston, Birmingham B15 2TT, United Kingdom
    DNA Repair (Amst) 12:588-99. 2013
    ..Therefore, this review aims to address the question: Is defective DNA double strand break repair an underlying cause of neurodegeneration? ..
  14. doi request reprint BOD1L Is Required to Suppress Deleterious Resection of Stressed Replication Forks
    Martin R Higgs
    School of Cancer Sciences, University of Birmingham, Birmingham B15 2TT, UK
    Mol Cell 59:462-77. 2015
    ..Thus, our work implicates BOD1L as a critical regulator of genome integrity that restrains nucleolytic degradation of damaged replication forks. ..
  15. doi request reprint DNA double-strand break repair, immunodeficiency and the RIDDLE syndrome
    Rachel M Blundred
    School of Cancer Sciences, University of Birmingham, Vincent Drive, Edgbaston, Birmingham, B15 2TT, UK
    Expert Rev Clin Immunol 7:169-85. 2011
    ..We also consider the implications of this finding on the mechanisms controlling development of the immune system...
  16. pmc A Hypomorphic PALB2 Allele Gives Rise to an Unusual Form of FA-N Associated with Lymphoid Tumour Development
    Philip J Byrd
    Institute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, United Kingdom
    PLoS Genet 12:e1005945. 2016
    ..We conclude that a very mild form of FA-N exists arising from a hypomorphic PALB2 allele. ..
  17. ncbi request reprint The APC/C and CBP/p300 cooperate to regulate transcription and cell-cycle progression
    Andrew S Turnell
    Cancer Research UK Institute for Cancer Studies, The Medical School, The University of Birmingham, Edgbaston, Birmingham B15 2TT, UK
    Nature 438:690-5. 2005
    ..Taken together, our results define discrete roles for the APC/C-CBP/p300 complexes in growth regulation...
  18. pmc Activation of DNA Damage Response Pathways during Lytic Replication of KSHV
    Robert Hollingworth
    School of Cancer Sciences, the College of Medicine and Dentistry, University of Birmingham, Birmingham B15 2TT, UK
    Viruses 7:2908-27. 2015
    ..KSHV appears then to selectively activate DDR pathways, modulate cell cycle progression and recruit DDR proteins to sites of viral replication during the lytic cycle...
  19. pmc Damaged replication forks tolerate USP7 to maintain genome stability
    Anastasia Zlatanou
    School of Cancer Sciences, University of Birmingham, Birmingham, UK
    Mol Cell Oncol 3:e1063571. 2016
    ..Recently, we have identified the deubiquitylating enzyme USP7 as a component of the DTT machinery that acts to protect RAD18 from proteasome-dependent degradation. ..
  20. pmc Protection or resection: BOD1L as a novel replication fork protection factor
    Martin R Higgs
    a Institute of Cancer and Genomic Studies, University of Birmingham, Birmingham, UK
    Nucleus 7:34-40. 2016
    ....
  21. doi request reprint A single strand that links multiple neuropathologies in human disease
    John J Reynolds
    School of Cancer Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TT, UK
    Brain 136:14-27. 2013
    ..presents several hypotheses based on current literature on a number of important questions, in particular, how do mutations in different end processing factors within the same DNA repair pathway lead to such different neuropathologies?..
  22. doi request reprint A PIAS-ed view of DNA double strand break repair focuses on SUMO
    Anastasia Zlatanou
    School of Cancer Sciences, University of Birmingham, Vincent Drive, Edgbaston, Birmingham, West Midlands B15 2TT, UK
    DNA Repair (Amst) 9:588-92. 2010
    ..Two recent papers highlight the importance of SUMO modifications of proteins that execute the response to DNA damage...
  23. pmc Constitutive phosphorylation of MDC1 physically links the MRE11-RAD50-NBS1 complex to damaged chromatin
    Christoph Spycher
    Institute of Veterinary Biochemistry and Molecular Biology, University of Zurich, 8057 Zurich, Switzerland
    J Cell Biol 181:227-40. 2008
    ..Thus, our data reveal the mechanism by which MDC1 physically couples the MRN complex to damaged chromatin...
  24. pmc Human Claspin works with BRCA1 to both positively and negatively regulate cell proliferation
    Shiaw Yih Lin
    Verna and Marrs McLean Department of Biochemistry, Baylor College of Medicine, Houston, TX 77030, USA
    Proc Natl Acad Sci U S A 101:6484-9. 2004
    ..These results suggest that Claspin has properties of both a tumor suppressor and an oncogene...