Blake D Anson
Affiliation: University of Wisconsin
- Pharmacological rescue of human K(+) channel long-QT2 mutations: human ether-a-go-go-related gene rescue without blockSridharan Rajamani
Department of Medicine, University of Wisconsin, Madison, USA
Circulation 105:2830-5. 2002..The G601S mutation was also rescued without channel block...
- Molecular and functional characterization of common polymorphisms in HERG (KCNH2) potassium channelsBlake D Anson
Department of Medicine, University of Wisconsin, 1300 University Ave, Madison, WI 53711, USA
Am J Physiol Heart Circ Physiol 286:H2434-41. 2004..All HERG channels had similar sensitivity to block by cisapride. Therefore, some HERG polymorphic channels are electrophysiologically different from WT channels...
- Most LQT2 mutations reduce Kv11.1 (hERG) current by a class 2 (trafficking-deficient) mechanismCorey L Anderson
Department of Medicine, University of Wisconsin Madison, WI, USA
Circulation 113:365-73. 2006..1 current (IKv11.1). We tested the hypotheses that (1) most LQT2 missense mutations generate trafficking-deficient Kv11.1 channels, and (2) their trafficking-deficient phenotype can be corrected...
- Properties of WT and mutant hERG K(+) channels expressed in neonatal mouse cardiomyocytesEric C Lin
Section of Cardiovascular Medicine, Departments of Medicine and Physiology, University of Wisconsin, Madison, Wisconsin, USA
Am J Physiol Heart Circ Physiol 298:H1842-9. 2010..An important finding of this work is that pharmacological correction of trafficking-deficient LQT2 mutations, as a potential innovative approach to therapy, is possible in native cardiac tissue...
- Intragenic suppression of trafficking-defective KCNH2 channels associated with long QT syndromeBrian P Delisle
Department of Medicine, University of Wisconsin, Madison, Wisconsin 53706, USA
Mol Pharmacol 68:233-40. 2005..These are the first findings to demonstrate that a single amino acid substitution in the putative KCNH2 drug binding domain can cause intragenic suppression of several LQT2 mutations...
- Thapsigargin selectively rescues the trafficking defective LQT2 channels G601S and F805CBrian P Delisle
Department of Medicine Cardiology, University of Wisconsin, Madison, Wisconsin 53706, USA
J Biol Chem 278:35749-54. 2003..e. LQT2 and cystic fibrosis)...
- Blockade of HERG channels by HIV protease inhibitorsBlake D Anson
Department of Medicine, University of Wisconsin Madison, Madison, WI, USA
Lancet 365:682-6. 2005..Our data show that four protease inhibitors block HERG channels, suggesting that protease inhibitors could predispose individuals to QT prolongation and torsade de pointes...
- High purity human-induced pluripotent stem cell-derived cardiomyocytes: electrophysiological properties of action potentials and ionic currentsJunyi Ma
Cellular Dynamics International, Madison, Wisconsin, USA
Am J Physiol Heart Circ Physiol 301:H2006-17. 2011..These hiPSC-derived cardiomyocytes have the added advantage that they can be used in high-throughput assays, and they have the potential to impact multiple areas of cardiovascular research and therapeutic applications...
- Biology of cardiac arrhythmias: ion channel protein traffickingBrian P Delisle
Section of Cardiovascular Medicine, Department of Medicine, University of Wisconsin Madison, USA
Circ Res 94:1418-28. 2004..As a scientist and physician, his writings and mentorship have served to foster a generation of investigators who continue to bring this complex field toward greater scientific understanding and impact on humankind...
- Specific serine proteases selectively damage KCNH2 (hERG1) potassium channels and I(Kr)Sridharan Rajamani
Department of Medicine Cardiology, University of Wisconsin, Madison 53792, USA
Am J Physiol Heart Circ Physiol 290:H1278-88. 2006....
- Genetic basis for the origin of cardiac arrhythmias: implications for therapyMackenzi Mbai
University of Wisconsin Hospitals and Clinics, Section of Cardiovascular Medicine, Room H6 354 CSC 3248, 600 Highland Avenue, Madison, WI 53792, USA
Curr Cardiol Rep 4:411-7. 2002..New therapies based on this evolving insight are being developed. This review summarizes recent discoveries with a focus on the genetic basis of cardiac arrhythmias and their implications for new therapies...
- An intronic mutation causes long QT syndromeLi Zhang
LDS Hospital, Salt Lake City, Utah 84103, USA
J Am Coll Cardiol 44:1283-91. 2004..The purpose of this research was to determine whether an intronic variant (T1945+6C) in KCNH2 is a disease-causing mutation, and if expanded phenotyping criteria produce improved identification of long QT syndrome (LQTS) patients...
- Comparison of HERG channel blocking effects of various beta-blockers-- implication for clinical strategyKazunobu Kawakami
Second Department of Internal Medicine, University of Occupational and Environmental Health Japan, 1 1 Iseigaoka, Kitakyushu 807 8555, Japan
Br J Pharmacol 147:642-52. 2006..Carvedilol has a class III antiarrhythmic effect, which may provide the rationale for a favourable clinical outcome compared with other beta-blockers as suggested in the recent COMET (Carvedilol Or Metoprolol European Trial) substudy...
- Molecular characterization, functional expression, and developmental profile of an ether à-go-go K+ channel in the tobacco hornworm Manduca sextaMatthew R Keyser
Department of Biological Sciences, P O Box 413, University of Wisconsin Milwaukee, Milwaukee, Wisconsin 53201, USA
J Neurobiol 55:73-85. 2003..These results provide the foundation for functional and modulatory studies of the Eag family of K+ channels in Manduca, which will complement the genetic analysis in Drosophila...