Genomes and Genes
Roger S Y Foo
Affiliation: University of Cambridge
- Nutrient deprivation regulates DNA damage repair in cardiomyocytes via loss of the base-excision repair enzyme OGG1Lee 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...
- High-throughput sequencing identifies STAT3 as the DNA-associated factor for p53-NF-kappaB-complex-dependent gene expression in human heart failureMun 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...
- Ubiquitination and degradation of the anti-apoptotic protein ARC by MDM2Roger 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...
- Elevated InsP3R expression underlies enhanced calcium fluxes and spontaneous extra-systolic calcium release events in hypertrophic cardiac myocytesDagmar Harzheim
Department of Molecular Signaling, Babraham Institute, Cambridge, UK
Channels (Austin) 4:67-71. 2010....
- Genome-wide conserved consensus transcription factor binding motifs are hyper-methylatedMun 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...
- PKB/Akt activation inhibits p53-mediated HIF1A degradation that is independent of MDM2Mun 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...
- Differential DNA methylation correlates with differential expression of angiogenic factors in human heart failureMehregan Movassagh
Division of Cardiovascular Medicine, Addenbrooke s Centre for Clinical Investigation, University of Cambridge, Cambridge, United Kingdom
PLoS ONE 5:e8564. 2010....
- Distinct epigenomic features in end-stage failing human heartsMehregan 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...
- Simplified apoptotic cascadesMehregan 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...
- Increased InsP3Rs in the junctional sarcoplasmic reticulum augment Ca2+ transients and arrhythmias associated with cardiac hypertrophyDagmar 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...
- Heme oxygenase-1 gene transfer inhibits angiotensin II-mediated rat cardiac myocyte apoptosis but not hypertrophyRoger 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...