Genomes and Genes
Grant S Stewart
Affiliation: University of Birmingham
- MDC1 is a mediator of the mammalian DNA damage checkpointGrant 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...
- Ataxia telangiectasia mutated-deficient B-cell chronic lymphocytic leukemia occurs in pregerminal center cells and results in defective damage response and unrepaired chromosome damageTatjana Stankovic
University of Birmingham, CRC Institute for Cancer Studies, The Medical School, Edgbaston, United Kingdom
Blood 99:300-9. 2002....
- Variations in ATM protein expression during normal lymphoid differentiation and among B-cell-derived neoplasiasJane 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...
- 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 responsesTatjana 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...
- The RIDDLE syndrome protein mediates a ubiquitin-dependent signaling cascade at sites of DNA damageGrant 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...
- RIDDLE immunodeficiency syndrome is linked to defects in 53BP1-mediated DNA damage signalingGrant 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...
- Solving the RIDDLE of 53BP1 recruitment to sites of damageGrant S Stewart
Cancer Research UK Institute for Cancer Studies, University of Birmingham, Edgbaston, Birmingham, UK
Cell Cycle 8:1532-8. 2009....
- Mediator of DNA damage checkpoint 1 (MDC1) regulates mitotic progressionKelly 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...
- Adenovirus 12 E4orf6 inhibits ATR activation by promoting TOPBP1 degradationAndrew 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...
- Serotype-specific inactivation of the cellular DNA damage response during adenovirus infectionNatalie 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...
- Adenovirus E4orf3 targets transcriptional intermediary factor 1γ for proteasome-dependent degradation during infectionNatalie 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...
- A role for E1B-AP5 in ATR signaling pathways during adenovirus infectionAndrew 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...
- DNA double-strand break repair, immunodeficiency and the RIDDLE syndromeRachel 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...
- The APC/C and CBP/p300 cooperate to regulate transcription and cell-cycle progressionAndrew 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...
- A nervous predisposition to unrepaired DNA double strand breaksJohn 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? ..
- A single strand that links multiple neuropathologies in human diseaseJohn 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?..
- A PIAS-ed view of DNA double strand break repair focuses on SUMOAnastasia 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...
- Constitutive phosphorylation of MDC1 physically links the MRE11-RAD50-NBS1 complex to damaged chromatinChristoph 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...
- Human Claspin works with BRCA1 to both positively and negatively regulate cell proliferationShiaw 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...