Jason I E Bruce

Summary

Affiliation: University of Rochester
Country: USA

Publications

  1. ncbi Phosphorylation of inositol 1,4,5-trisphosphate receptors in parotid acinar cells. A mechanism for the synergistic effects of cAMP on Ca2+ signaling
    Jason I E Bruce
    Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Biol Chem 277:1340-8. 2002
  2. ncbi Ca2+-dependent protein kinase--a modulation of the plasma membrane Ca2+-ATPase in parotid acinar cells
    Jason I E Bruce
    Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, New York 14642, USA
    J Biol Chem 277:48172-81. 2002
  3. ncbi A role for phosphorylation of inositol 1,4,5-trisphosphate receptors in defining calcium signals induced by Peptide agonists in pancreatic acinar cells
    Stephen V Straub
    Department of Pharmacology and Physiology, University of Rochester, Rochester, New York 14642, USA
    J Biol Chem 277:31949-56. 2002
  4. ncbi cAMP potentiates ATP-evoked calcium signaling in human parotid acinar cells
    David A Brown
    Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Biol Chem 279:39485-94. 2004
  5. ncbi Modulation of cytosolic calcium signaling by protein kinase A-mediated phosphorylation of inositol 1,4,5-trisphosphate receptors
    Stephen V Straub
    University of Rochester, Department of Pharmacology and Physiology, School of Medicine and Dentistry, Rochester, New York 14642, USA
    Biol Res 37:593-602. 2004
  6. ncbi Modulation of [Ca2+]i signaling dynamics and metabolism by perinuclear mitochondria in mouse parotid acinar cells
    Jason I E Bruce
    Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    J Biol Chem 279:12909-17. 2004
  7. ncbi Crosstalk between cAMP and Ca2+ signaling in non-excitable cells
    Jason I E Bruce
    Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Cell Calcium 34:431-44. 2003
  8. ncbi Cytosolic Ca(2+) and Ca(2+)-activated Cl(-) current dynamics: insights from two functionally distinct mouse exocrine cells
    David R Giovannucci
    Department of Pharmacology and Physiology, University of Rochester, School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642, USA
    J Physiol 540:469-84. 2002
  9. ncbi Oxidant-impaired intracellular Ca2+ signaling in pancreatic acinar cells: role of the plasma membrane Ca2+-ATPase
    Jason I E Bruce
    Faculty of Life Sciences, 2nd Floor Core Technology Facility, 46 Grafton St, The Univ of Manchester, Manchester M13 9NT, UK
    Am J Physiol Cell Physiol 293:C938-50. 2007
  10. ncbi Differential regulation of the apical plasma membrane Ca(2+) -ATPase by protein kinase A in parotid acinar cells
    Erin Baggaley
    Faculty of Life Sciences, The University of Manchester, Manchester, UK
    J Biol Chem 282:37678-93. 2007

Collaborators

Detail Information

Publications10

  1. ncbi Phosphorylation of inositol 1,4,5-trisphosphate receptors in parotid acinar cells. A mechanism for the synergistic effects of cAMP on Ca2+ signaling
    Jason I E Bruce
    Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Biol Chem 277:1340-8. 2002
    ..In addition, this report supports the emerging consensus that phosphorylation at the level of the Ca(2+) release machinery is a broadly important mechanism by which cells can regulate Ca(2+)-mediated processes...
  2. ncbi Ca2+-dependent protein kinase--a modulation of the plasma membrane Ca2+-ATPase in parotid acinar cells
    Jason I E Bruce
    Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, New York 14642, USA
    J Biol Chem 277:48172-81. 2002
    ..Tight regulation of both Ca(2+) release and Ca(2+) efflux may represent a general feature of the mechanism whereby cAMP improves the fidelity and specificity of Ca(2+) signaling...
  3. ncbi A role for phosphorylation of inositol 1,4,5-trisphosphate receptors in defining calcium signals induced by Peptide agonists in pancreatic acinar cells
    Stephen V Straub
    Department of Pharmacology and Physiology, University of Rochester, Rochester, New York 14642, USA
    J Biol Chem 277:31949-56. 2002
    ..Thus, we conclude that PKA-mediated phosphorylation of type III InsP(3)R is a general mechanism by which the patterns of [Ca(2+)](c) oscillations are shaped in pancreatic acinar cells...
  4. ncbi cAMP potentiates ATP-evoked calcium signaling in human parotid acinar cells
    David A Brown
    Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Biol Chem 279:39485-94. 2004
    ..These data indicate that in human parotid acinar cells, in addition to modulation of Ca(2+) release, Ca(2+) influx through P2X(4)R may constitute a further locus for the synergistic effects of Ca(2+) and PKA activation...
  5. ncbi Modulation of cytosolic calcium signaling by protein kinase A-mediated phosphorylation of inositol 1,4,5-trisphosphate receptors
    Stephen V Straub
    University of Rochester, Department of Pharmacology and Physiology, School of Medicine and Dentistry, Rochester, New York 14642, USA
    Biol Res 37:593-602. 2004
    ..This review will focus on recent advances in our understanding of phosphoregulation of InsP3R, as well as the functional consequences of this modulation in terms of eliciting specific cellular events...
  6. ncbi Modulation of [Ca2+]i signaling dynamics and metabolism by perinuclear mitochondria in mouse parotid acinar cells
    Jason I E Bruce
    Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    J Biol Chem 279:12909-17. 2004
    ..These effects may profoundly affect a variety of nuclear processes in parotid acinar cells while facilitating efficient fluid secretion...
  7. ncbi Crosstalk between cAMP and Ca2+ signaling in non-excitable cells
    Jason I E Bruce
    Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Cell Calcium 34:431-44. 2003
    ..This review will focus on the predominant molecular loci at which these classical signaling systems interact to impact the spatio-temporal pattern of [Ca2+](i) signaling in non-excitable cells...
  8. ncbi Cytosolic Ca(2+) and Ca(2+)-activated Cl(-) current dynamics: insights from two functionally distinct mouse exocrine cells
    David R Giovannucci
    Department of Pharmacology and Physiology, University of Rochester, School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642, USA
    J Physiol 540:469-84. 2002
    ..These data reveal specializations of common modules of Ca(2+)-release machinery and subsequent effector activation that are specifically suited to the distinct functional roles of these two related cell types...
  9. ncbi Oxidant-impaired intracellular Ca2+ signaling in pancreatic acinar cells: role of the plasma membrane Ca2+-ATPase
    Jason I E Bruce
    Faculty of Life Sciences, 2nd Floor Core Technology Facility, 46 Grafton St, The Univ of Manchester, Manchester M13 9NT, UK
    Am J Physiol Cell Physiol 293:C938-50. 2007
    ..1-1 mM) inactivated the plasma membrane Ca(2+)-ATPase. This may be important in facilitating "Ca(2+) overload," resulting in cell injury associated with pancreatitis...
  10. ncbi Differential regulation of the apical plasma membrane Ca(2+) -ATPase by protein kinase A in parotid acinar cells
    Erin Baggaley
    Faculty of Life Sciences, The University of Manchester, Manchester, UK
    J Biol Chem 282:37678-93. 2007
    ..Such tight spatial regulation of Ca(2+) efflux is likely important for the fine-tuning of Ca(2+)-dependent effectors close to the apical membrane important for the regulation of fluid secretion and exocytosis...