JOHN BRIDGE

Summary

Affiliation: University of Utah
Country: USA

Publications

  1. pmc New insights into the structure and function of couplons
    John H B Bridge
    Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT, USA
    J Physiol 586:3735. 2008
  2. pmc Revealing the cellular basis of heart failure
    John 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
  3. pmc Effect of metabolic inhibition on couplon behavior in rabbit ventricular myocytes
    Chana Chantawansri
    Division of Cardiology, Cardiovascular Research Laboratories, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
    Biophys J 94:1656-66. 2008
  4. pmc Variability in couplon size in rabbit ventricular myocytes
    Masashi 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
  5. ncbi request reprint Ca2+ sparks in rabbit ventricular myocytes evoked by action potentials: involvement of clusters of L-type Ca2+ channels
    Masashi 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
  6. pmc Novel features of the rabbit transverse tubular system revealed by quantitative analysis of three-dimensional reconstructions from confocal images
    Eleonora 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
  7. ncbi request reprint A novel mechanism of pacemaker control that depends on high levels of cAMP and PKA-dependent phosphorylation: a precisely controlled biological clock
    John H B Bridge
    Circ Res 98:437-9. 2006
  8. ncbi request reprint Metabolic inhibition alters subcellular calcium release patterns in rat ventricular myocytes: implications for defective excitation-contraction coupling during cardiac ischemia and failure
    Gary 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
  9. pmc Allosteric activation of Na+-Ca2+ exchange by L-type Ca2+ current augments the trigger flux for SR Ca2+ release in ventricular myocytes
    Eric A Sobie
    Biophys J 94:L54-6. 2008
  10. ncbi request reprint 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

Research Grants

Collaborators

Detail Information

Publications10

  1. pmc New insights into the structure and function of couplons
    John H B Bridge
    Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT, USA
    J Physiol 586:3735. 2008
  2. pmc Revealing the cellular basis of heart failure
    John 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
  3. pmc Effect of metabolic inhibition on couplon behavior in rabbit ventricular myocytes
    Chana 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...
  4. pmc Variability in couplon size in rabbit ventricular myocytes
    Masashi 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...
  5. ncbi request reprint Ca2+ sparks in rabbit ventricular myocytes evoked by action potentials: involvement of clusters of L-type Ca2+ channels
    Masashi 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...
  6. pmc Novel features of the rabbit transverse tubular system revealed by quantitative analysis of three-dimensional reconstructions from confocal images
    Eleonora 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...
  7. ncbi request reprint A novel mechanism of pacemaker control that depends on high levels of cAMP and PKA-dependent phosphorylation: a precisely controlled biological clock
    John H B Bridge
    Circ Res 98:437-9. 2006
  8. ncbi request reprint Metabolic inhibition alters subcellular calcium release patterns in rat ventricular myocytes: implications for defective excitation-contraction coupling during cardiac ischemia and failure
    Gary 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...
  9. pmc Allosteric activation of Na+-Ca2+ exchange by L-type Ca2+ current augments the trigger flux for SR Ca2+ release in ventricular myocytes
    Eric 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...
  10. ncbi request reprint 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

Research Grants9

  1. NON LINEAR EFFECTS OF SR RELEASE TRIGGERS IN HEART
    JOHN BRIDGE; Fiscal Year: 2002
    ..Finally the effect of Na, Na-Ca exchange and controlled Na currents on microscopic gain will be tested. ..
  2. RELATIONSHIPS BETWEEN SPARKS AND THEIR TRIGGERS IN HEART
    JOHN BRIDGE; Fiscal Year: 2007
    ..Methods include measuring sparks and cell morphology with a combination of antibodies and mathematical deconvolution techniques. ..