Jason L Scragg
Affiliation: University of Leeds
- Constitutive activity of human angiotensin II type-1 receptors by Gq overexpressionJason L Scragg
CRISTAL Cardiovascular Research Institute at Leeds, School of Medicine, University of Leeds, Leeds LS2 9JT, UK
Biochem Biophys Res Commun 334:134-9. 2005..The data suggest that the resting equilibrium of hAT(1) receptors between the inactive (R) and active (R*) forms is predominantly weighted towards the inactive conformation...
- Carbon monoxide inhibits L-type Ca2+ channels via redox modulation of key cysteine residues by mitochondrial reactive oxygen speciesJason L Scragg
Division of Cardiovascular and Neuronal Remodelling, Leeds Institute of Genetics, Health, and Therapeutics, Level 10, Worsley Bldg, University of Leeds, Leeds LS2 9JT, United Kingdom
J Biol Chem 283:24412-9. 2008..This in turn leads to redox modulation of any or all of three critical cysteine residues in the channel's cytoplasmic C-terminal tail, resulting in channel inhibition...
- Constitutive activity of endogenous receptors by inducible Gq overexpressionJason L Scragg
Cardiovascular Research Institute at Leeds, School of Medicine, University of Leeds, Leeds LS2 9JT, UK
Biochem Biophys Res Commun 331:1239-44. 2005..An inducible cell line, transiently expressing G proteins, can therefore be employed to induce constitutive activity of endogenously expressed GPCRs. This model system could be used to identify clinically important inverse agonists...
- Molecular requirements for L-type Ca2+ channel blockade by testosteroneJason L Scragg
Institute for Cardiovascular Research, School of Medicine, University of Leeds, Leeds LS2 9JT, UK
Cell Calcium 42:11-5. 2007....
- Carbon monoxide mediates the anti-apoptotic effects of heme oxygenase-1 in medulloblastoma DAOY cells via K+ channel inhibitionMoza M A Al-Owais
Division of Cardiovascular and Neuronal Remodelling, Light, Faculty of Medicine and Health, University of Leeds LS2 9JT, United Kingdom
J Biol Chem 287:24754-64. 2012....
- Modulation of hTREK-1 by carbon monoxideMark L Dallas
Faculty of Medicine and Health, University of Leeds, Leeds LS2 9JT, UK
Neuroreport 19:345-8. 2008..As both NO and CO are important neuronal gasotransmitters and TREK is crucial in regulating neuronal excitability, our results provide a novel means by which these gases may modulate neuronal activity...
- Cellular consequences of the expression of Alzheimer's disease-causing presenilin 1 mutations in human neuroblastoma (SH-SY5Y) cellsJohn P Boyle
Division of Cardiovascular and Neuronal Remodelling, Leeds Institute of Genetics, Health and Therapeutics, University of Leeds, Leeds, UK
Brain Res 1443:75-88. 2012..This, rather than any potential disruption of ER Ca(2+) stores, is likely to explain the extreme pathology of this mutant...
- Hypoxia and neurodegenerationChris Peers
Faculties of Medicine, University of Leeds, Leeds, United Kingdom
Ann N Y Acad Sci 1177:169-77. 2009..However, it remains to be determined whether inhibition of one or more of the effects of hypoxia may be of benefit in arresting the development of this neurodegenerative disease...
- Carbon monoxide protects against oxidant-induced apoptosis via inhibition of Kv2.1Mark L Dallas
Division of Cardiovascular and Neuronal Remodelling, Faculty of Medicine and Health, University of Leeds, Leeds, UK
FASEB J 25:1519-30. 2011..Our results provide a novel mechanism to account for the neuroprotective effects of CO against oxidative apoptosis, which has potential for therapeutic exploitation to provide neuronal protection in situations of oxidative stress...
- H2O 2-stimulated Ca2+ influx via TRPM2 is not the sole determinant of subsequent cell deathJenny A Wilkinson
School of Medicine, University of Leeds, Leeds LS2 9JT, UK
Pflugers Arch 455:1141-51. 2008....
- Carbon Monoxide Induces Cardiac Arrhythmia via Induction of the Late Na+ CurrentMark L Dallas
Division of Cardiovascular and Neuronal Remodelling, Light, Faculty of Medicine and Health, University of Leeds, Clarendon Way, Leeds LS2 9JT, UK
Am J Respir Crit Care Med 186:648-56. 2012..5 and to induction of the late Na(+) current. We also show that the antianginal drug ranolazine can abolish CO-induced early after-depolarizations, highlighting a novel approach to the treatment of CO-induced arrhythmias...
- A central role for ROS in the functional remodelling of L-type Ca2+ channels by hypoxiaChris Peers
University of Leeds School of Medicine Worsley Building, Leeds LS2 9JT, UK
Philos Trans R Soc Lond B Biol Sci 360:2247-54. 2005..We suggest, therefore, that our data provide a cellular basis to account for the known increased incidence of Alzheimer's disease in patients who have suffered prolonged hypoxic episodes...
- Testosterone is a potent inhibitor of L-type Ca(2+) channelsJason L Scragg
Institute for Cardiovascular Research, University of Leeds, Leeds LS2 9JT, UK
Biochem Biophys Res Commun 318:503-6. 2004..This effect is likely to account for its beneficial cardiovascular actions...
- Modulation of ion channels by hydrogen sulfideChris Peers
Division of Cardiovascular and Neuronal Remodelling, Faculty of Medicine and Health, Leeds Institute for Genetics Health and Therapeutics, University of Leeds, Leeds, United Kingdom
Antioxid Redox Signal 17:95-105. 2012..In addition, more sensitive methods for detecting relevant physiological concentrations of H(2)S will allow for clarification of specific ion channel regulation with reference to physiological or pathophysiological settings...
- Analysis of oxygen-sensitive human cardiac L-type Ca2+ channel alpha1C subunit (hHT Isoform)Jason L Scragg
Institute for Cardiovascular Research, University of Leeds, United Kingdom
Methods Enzymol 381:290-302. 2004
- Mitochondrial ROS production initiates Abeta1-40-mediated up-regulation of L-type Ca2+ channels during chronic hypoxiaIan M Fearon
Faculty of Life Sciences, The University of Manchester, Manchester M13 9PT, UK
Adv Exp Med Biol 580:197-201; discussion 351-9. 2006
- Hypoxic augmentation of Ca2+ channel currents requires a functional electron transport chainStephen T Brown
Department of Biology, McMaster University, 1280 Main Street West, Hamilton, Ontario L8S 4K1, Canada
J Biol Chem 280:21706-12. 2005..Thus oxidant production in the mitochondrial ETC is a critical factor, acting upstream of amyloid beta peptide production in the up-regulation of Ca(2+) channels in response to CH...
- Alzheimer's amyloid peptides mediate hypoxic up-regulation of L-type Ca2+ channelsJason L Scragg
Institute for Cardiovascular Research, The University of Leeds, Leeds, UK
FASEB J 19:150-2. 2005..Such an action will likely contribute to the Ca2+ dyshomeostasis of Alzheimer's disease and may contribute to the mechanisms underlying the known increased incidence of this neurodegenerative disease following hypoxic episodes...