S J Fuller
Affiliation: Imperial College
- Oncogenic src, raf, and ras stimulate a hypertrophic pattern of gene expression and increase cell size in neonatal rat ventricular myocytesS J Fuller
Section of Cardiac Medicine, National Heart and Lung Institute Division, Imperial College School of Medicine, London SW3 6LY, United Kingdom
J Biol Chem 273:18146-52. 1998..We conclude that members of the Src family of tyrosine kinases may be important in mediating the transcriptional changes occurring during cardiac myocyte hypertrophy and that Ras and Raf may be downstream effectors...
- Stimulation of gene expression in neonatal rat ventricular myocytes by Ras is mediated by Ral guanine nucleotide dissociation stimulator (Ral.GDS) and phosphatidylinositol 3-kinase in addition to RafS J Fuller
NHLI Division Cardiac Medicine, Imperial College School of Medicine, London SW3 6LY, UK
Biochem J 335:241-6. 1998..9-fold). These results suggest that Raf, Ral.GDS and PI-3-K can all transduce transcriptional responses to V12HRas, but that the specific induction of genes associated with the hypertrophic response is not mediated through PI-3-K...
- G alpha 13 stimulates gene expression and increases cell size in cultured neonatal rat ventricular myocytesS G Finn
NHL1 Division, Imperial College School of Medicine, London, UK
Cardiovasc Res 42:140-8. 1999..The objective of this study was to determine whether constitutively-active G alpha 13 is able to induce a hypertrophic phenotype in cardiac myocytes...
- Regulation of mitogen-activated protein kinases in cardiac myocytes through the small G protein Rac1A Clerk
Division of Biomedical Sciences Molecular Pathology Section, Imperial College School of Medicine, London SW7 2AZ, United Kingdom
Mol Cell Biol 21:1173-84. 2001..We conclude that activation of Rac1 by hypertrophic stimuli contributes to the hypertrophic response by modulating the ERK and/or possibly the JNK (but not the p38-MAPK) cascades...
- c-Jun N-terminal kinase-interacting protein 1 inhibits gene expression in response to hypertrophic agonists in neonatal rat ventricular myocytesS G Finn
NHLI Division (Cardiac Medicine, Imperial College School of Medicine, Dovehouse Street, London SW3 6LY, UK
Biochem J 358:489-95. 2001..These results suggest that activation of the JNK pathway contributes to the transcriptional and morphological responses to G(q) receptor-coupled hypertrophic agonists...
- Glycogen synthase kinase 3 (GSK3) in the heart: a point of integration in hypertrophic signalling and a therapeutic target? A critical analysisP H Sugden
National Heart and Lung Institute NHLI Division, Faculty of Medicine, Imperial College London, London, UK
Br J Pharmacol 153:S137-53. 2008..We discuss whether cardiac pathologies could be treated by therapeutic intervention at the GSK3 level but conclude that any intervention would be premature without greater understanding of the precise role of GSK3 in cardiac processes...
- Stimulation of "stress-regulated" mitogen-activated protein kinases (stress-activated protein kinases/c-Jun N-terminal kinases and p38-mitogen-activated protein kinases) in perfused rat hearts by oxidative and other stressesA Clerk
National Heart and Lung Institute Division, Imperial College School of Medicine, Royal Brompton Campus, London SW3 6LY, United Kingdom
J Biol Chem 273:7228-34. 1998..These data are consistent with a role for reactive oxygen species in the activation of SR-MAPKs during ischemia/reperfusion...
- Beta-adrenoceptor subtype dependence of chronotropy in mouse embryonic stem cell-derived cardiomyocytesN N Ali
NHLI Division, Imperial College London, Dovehouse St, London SW3 6LY, UK
Basic Res Cardiol 99:382-91. 2004..This study extends the characterisation of ESCM as a preparation for studying receptor pharmacology, and indicates that the beta1AR is the predominant subtype mediating increases in contraction rate in murine ESCM...