Affiliation: University of Utah
- New insights into the structure and function of couplonsJohn H B Bridge
Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT, USA
J Physiol 586:3735. 2008
- Revealing the cellular basis of heart failureJohn H B Bridge
Nora Eccles Harrison CardiovascularResearch and Training Institute, Division of Cardiology, University of Utah, Salt Lake City, Utah, USA
Biophys J 93:3731-2. 2007
- Effect of metabolic inhibition on couplon behavior in rabbit ventricular myocytesChana Chantawansri
Division of Cardiology, Cardiovascular Research Laboratories, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
Biophys J 94:1656-66. 2008..In addition, the results are consistent with loss of RyR activity, which can be mitigated under conditions likely to enlarge the trigger...
- Variability in couplon size in rabbit ventricular myocytesMasashi Inoue
Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, 95 South 2000 East, Salt Lake City, UT 84112 5000, USA
Biophys J 89:3102-10. 2005..The variation in spark probability and latency with location suggests that the couplon size, and hence the number of L-type Ca(2+) channels in a couplon is variable...
- Ca2+ sparks in rabbit ventricular myocytes evoked by action potentials: involvement of clusters of L-type Ca2+ channelsMasashi Inoue
Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, 95 South 2000 East Back, Salt Lake City, Utah 84112 5000, USA
Circ Res 92:532-8. 2003..We conclude that it is likely that a cluster of LCCs is involved in gating a cluster of ryanodine receptors at the beginning of an AP...
- Novel features of the rabbit transverse tubular system revealed by quantitative analysis of three-dimensional reconstructions from confocal imagesEleonora Savio-Galimberti
Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, Utah 84112, USA
Biophys J 95:2053-62. 2008..We also propose that our methods allow us to characterize pathological defects of the t-system, e.g., its remodeling as a result of heart failure...
- A novel mechanism of pacemaker control that depends on high levels of cAMP and PKA-dependent phosphorylation: a precisely controlled biological clockJohn H B Bridge
Circ Res 98:437-9. 2006
- Metabolic inhibition alters subcellular calcium release patterns in rat ventricular myocytes: implications for defective excitation-contraction coupling during cardiac ischemia and failureGary H Fukumoto
Department of Medicine, Cardiovascular Research Laboratories, Geffen School of Medicine at UCLA, Los Angeles, Calif 90095 1679, USA
Circ Res 96:551-7. 2005..We conclude that metabolic inhibition interferes with E-C coupling by (1) reducing trigger Ca2+, and (2) directly inhibiting sarcoplasmic reticulum Ca2+ release site open probability...
- Allosteric activation of Na+-Ca2+ exchange by L-type Ca2+ current augments the trigger flux for SR Ca2+ release in ventricular myocytesEric A Sobie
Biophys J 94:L54-6. 2008..These results help to resolve seemingly contradictory results obtained previously and have implications for our understanding of the triggering of Ca(2+) release in heart cells under various conditions...
- What are the consequences of phosphorylation and hyperphosphorylation of ryanodine receptors in normal and failing heart?John H B Bridge
Circ Res 102:995-7. 2008