Roger S Y Foo

Summary

Affiliation: University of Cambridge
Country: UK

Publications

  1. ncbi Nutrient deprivation regulates DNA damage repair in cardiomyocytes via loss of the base-excision repair enzyme OGG1
    Lee Siggens
    Division of Cardiovascular Medicine, University of Cambridge, Addenbrooke s Centre of Clinical Investigation Building, Level 6, Addenbrooke s Hospital, Cambridge, CB2 0QQ, UK
    FASEB J 26:2117-24. 2012
  2. ncbi High-throughput sequencing identifies STAT3 as the DNA-associated factor for p53-NF-kappaB-complex-dependent gene expression in human heart failure
    Mun Kit Choy
    Department of Medicine, University of Cambridge, Addenbrooke s Centre for Clinical Investigation, Hills Road, Cambridge, CB2 0QQ, UK
    Genome Med 2:37. 2010
  3. ncbi Ubiquitination and degradation of the anti-apoptotic protein ARC by MDM2
    Roger S Y Foo
    Division of Cardiovascular Medicine, University of Cambridge, Addenbrooke s Hospital, Cambridge CB2 2QQ, United Kingdom
    J Biol Chem 282:5529-35. 2007
  4. ncbi Elevated InsP3R expression underlies enhanced calcium fluxes and spontaneous extra-systolic calcium release events in hypertrophic cardiac myocytes
    Dagmar Harzheim
    Department of Molecular Signaling, Babraham Institute, Cambridge, UK
    Channels (Austin) 4:67-71. 2010
  5. ncbi Genome-wide conserved consensus transcription factor binding motifs are hyper-methylated
    Mun Kit Choy
    Department of Medicine, University of Cambridge, ACCI Building Level 6, Cambridge CB20QQ, UK
    BMC Genomics 11:519. 2010
  6. ncbi PKB/Akt activation inhibits p53-mediated HIF1A degradation that is independent of MDM2
    Mun Kit Choy
    Department of Medicine, University of Cambridge, Addenbrooke s Hospital, Cambridge CB2 20QQ, UK
    J Cell Physiol 222:635-9. 2010
  7. ncbi Differential DNA methylation correlates with differential expression of angiogenic factors in human heart failure
    Mehregan Movassagh
    Division of Cardiovascular Medicine, Addenbrooke s Centre for Clinical Investigation, University of Cambridge, Cambridge, United Kingdom
    PLoS ONE 5:e8564. 2010
  8. ncbi Distinct epigenomic features in end-stage failing human hearts
    Mehregan Movassagh
    Division of Cardiovascular Medicine, University of Cambridge, Addenbrooke s Centre for Clinical Investigation, Level 6, Hills Rd, Cambridge, CB2 0QQ UK
    Circulation 124:2411-22. 2011
  9. ncbi Simplified apoptotic cascades
    Mehregan Movassagh
    Division of Cardiovascular Medicine, Addenbrooke s Hospital, University of Cambridge, ACCI Building Level 6, Hills Road, Box 110, Cambridge CB2 2QQ, UK
    Heart Fail Rev 13:111-9. 2008
  10. ncbi Increased InsP3Rs in the junctional sarcoplasmic reticulum augment Ca2+ transients and arrhythmias associated with cardiac hypertrophy
    Dagmar Harzheim
    Department of Molecular Signaling, Babraham Institute, Cambridge, CB22 3AT, United Kingdom
    Proc Natl Acad Sci U S A 106:11406-11. 2009

Collaborators

  • Martin R Bennett
  • Mun Kit Choy
  • Thomas A Down
  • Morris J Brown
  • Mehregan Movassagh
  • Dagmar Harzheim
  • Lee Siggens
  • Nichola Figg
  • Martin Goddard
  • Martin D Bootman
  • H Llewelyn Roderick
  • Syed Haider
  • David A Knowles
  • Chris Penkett
  • Pietro Lio
  • Lina Cordeddu
  • Ilenia Simeoni
  • Ana Vujic
  • Amarnath Talasila
  • Stuart J Conway
  • Oliver Ritter
  • Aslam Tashfeen

Detail Information

Publications11

  1. ncbi Nutrient deprivation regulates DNA damage repair in cardiomyocytes via loss of the base-excision repair enzyme OGG1
    Lee Siggens
    Division of Cardiovascular Medicine, University of Cambridge, Addenbrooke s Centre of Clinical Investigation Building, Level 6, Addenbrooke s Hospital, Cambridge, CB2 0QQ, UK
    FASEB J 26:2117-24. 2012
    ..The manipulation of OGG1 may be used in future studies to examine the direct contribution of oxidative DNA damage to the progression of heart failure...
  2. ncbi High-throughput sequencing identifies STAT3 as the DNA-associated factor for p53-NF-kappaB-complex-dependent gene expression in human heart failure
    Mun Kit Choy
    Department of Medicine, University of Cambridge, Addenbrooke s Centre for Clinical Investigation, Hills Road, Cambridge, CB2 0QQ, UK
    Genome Med 2:37. 2010
    ..CONCLUSIONS : Our results uncover a mechanism by which transcription factors cooperate in a multi-molecular complex at a cis-regulatory element to control gene expression...
  3. ncbi Ubiquitination and degradation of the anti-apoptotic protein ARC by MDM2
    Roger S Y Foo
    Division of Cardiovascular Medicine, University of Cambridge, Addenbrooke s Hospital, Cambridge CB2 2QQ, United Kingdom
    J Biol Chem 282:5529-35. 2007
    ..We conclude that MDM2 is a critical regulator of ARC levels in cardiomyocytes. Prevention of MDM2-induced degradation of ARC represents a potential therapeutic target to prevent cardiomyocyte apoptosis...
  4. ncbi Elevated InsP3R expression underlies enhanced calcium fluxes and spontaneous extra-systolic calcium release events in hypertrophic cardiac myocytes
    Dagmar Harzheim
    Department of Molecular Signaling, Babraham Institute, Cambridge, UK
    Channels (Austin) 4:67-71. 2010
    ....
  5. ncbi Genome-wide conserved consensus transcription factor binding motifs are hyper-methylated
    Mun Kit Choy
    Department of Medicine, University of Cambridge, ACCI Building Level 6, Cambridge CB20QQ, UK
    BMC Genomics 11:519. 2010
    ..We hypothesize that DNA methylation at conserved consensus motifs prevents promiscuous or disorderly transcription factor binding...
  6. ncbi PKB/Akt activation inhibits p53-mediated HIF1A degradation that is independent of MDM2
    Mun Kit Choy
    Department of Medicine, University of Cambridge, Addenbrooke s Hospital, Cambridge CB2 20QQ, UK
    J Cell Physiol 222:635-9. 2010
    ..In summary, we propose that p53-induced HIF1A degradation is not exclusively MDM2-mediated, but reversible by PKB/Akt phosphorylation...
  7. ncbi Differential DNA methylation correlates with differential expression of angiogenic factors in human heart failure
    Mehregan Movassagh
    Division of Cardiovascular Medicine, Addenbrooke s Centre for Clinical Investigation, University of Cambridge, Cambridge, United Kingdom
    PLoS ONE 5:e8564. 2010
    ....
  8. ncbi Distinct epigenomic features in end-stage failing human hearts
    Mehregan Movassagh
    Division of Cardiovascular Medicine, University of Cambridge, Addenbrooke s Centre for Clinical Investigation, Level 6, Hills Rd, Cambridge, CB2 0QQ UK
    Circulation 124:2411-22. 2011
    ..A consistent profile of gene expression changes in end-stage cardiomyopathy led us to hypothesize that distinct global patterns of the epigenome may also exist...
  9. ncbi Simplified apoptotic cascades
    Mehregan Movassagh
    Division of Cardiovascular Medicine, Addenbrooke s Hospital, University of Cambridge, ACCI Building Level 6, Hills Road, Box 110, Cambridge CB2 2QQ, UK
    Heart Fail Rev 13:111-9. 2008
    ..Understanding the intricacies of apoptotic death pathways and determining the relevance of these to cardiomyopathy is therefore essential if cardiomyocyte apoptosis is to be a pharmacological target for heart failure therapy...
  10. ncbi Increased InsP3Rs in the junctional sarcoplasmic reticulum augment Ca2+ transients and arrhythmias associated with cardiac hypertrophy
    Dagmar Harzheim
    Department of Molecular Signaling, Babraham Institute, Cambridge, CB22 3AT, United Kingdom
    Proc Natl Acad Sci U S A 106:11406-11. 2009
    ..Our data establish that increased InsP(3)R expression is a general mechanism that underlies remodeling of Ca(2+) signaling during heart disease, and in particular, in triggering ventricular arrhythmia during hypertrophy...
  11. ncbi Heme oxygenase-1 gene transfer inhibits angiotensin II-mediated rat cardiac myocyte apoptosis but not hypertrophy
    Roger S Y Foo
    Division of Cardiovascular Medicine, School of Clinical Medicine, Addenbrooke s Hospital, University of Cambridge, UK
    J Cell Physiol 209:1-7. 2006
    ..Our findings identify the signalling pathways by which HO-1 gene transfer protects against apoptosis and suggest that overexpression of HO-1 in cardiomyopathies may delay the transition from myocyte hypertrophy to heart failure...