David I Yule

Summary

Affiliation: University of Rochester
Country: USA

Publications

  1. pmc Linking structure to function: Recent lessons from inositol 1,4,5-trisphosphate receptor mutagenesis
    David I Yule
    Department of Pharmacology and Physiology, University of Rochester, NY, United States
    Cell Calcium 47:469-79. 2010
  2. ncbi request reprint Modulation of Ca2+ oscillations by phosphorylation of Ins(1,4,5)P3 receptors
    D I Yule
    Department of Pharmacology and Physiology, University of Rochester Medical School, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Biochem Soc Trans 31:954-7. 2003
  3. ncbi request reprint Critical role for NHE1 in intracellular pH regulation in pancreatic acinar cells
    David A Brown
    Dept of Pharmacology and Physiology, School of Medicine and Dentistry, Univ of Rochester Medical Center, 601 Elmwood Ave, Rochester, NY 14642, USA
    Am J Physiol Gastrointest Liver Physiol 285:G804-12. 2003
  4. pmc Functional inositol 1,4,5-trisphosphate receptors assembled from concatenated homo- and heteromeric subunits
    Kamil J Alzayady
    From the Department of Pharmacology and Physiology, University of Rochester, Rochester, New York 14642
    J Biol Chem 288:29772-84. 2013
  5. pmc ATP regulation of type-1 inositol 1,4,5-trisphosphate receptor activity does not require walker A-type ATP-binding motifs
    Matthew J Betzenhauser
    Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Biol Chem 284:16156-63. 2009
  6. ncbi request reprint 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
  7. ncbi request reprint 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
  8. ncbi request reprint 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
  9. pmc The type 2 inositol (1,4,5)-trisphosphate (InsP3) receptor determines the sensitivity of InsP3-induced Ca2+ release to ATP in pancreatic acinar cells
    Hyung Seo Park
    Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Biol Chem 283:26081-8. 2008
  10. pmc Tumor necrosis factor-alpha potentiates intraneuronal Ca2+ signaling via regulation of the inositol 1,4,5-trisphosphate receptor
    KEIGAN M PARK
    Center for Neural Development and Disease, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Biol Chem 283:33069-79. 2008

Collaborators

Detail Information

Publications46

  1. pmc Linking structure to function: Recent lessons from inositol 1,4,5-trisphosphate receptor mutagenesis
    David I Yule
    Department of Pharmacology and Physiology, University of Rochester, NY, United States
    Cell Calcium 47:469-79. 2010
    ..In addition, we review studies defining the structural requirements in the channel domain which comprise the conduction pathway and are suggested to be involved in the gating of the channel...
  2. ncbi request reprint Modulation of Ca2+ oscillations by phosphorylation of Ins(1,4,5)P3 receptors
    D I Yule
    Department of Pharmacology and Physiology, University of Rochester Medical School, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Biochem Soc Trans 31:954-7. 2003
    ..These data demonstrate that phosphoregulation of InsP(3)Rs results in subtype-specific effects and may play a role in the specificity of calcium signals by 'shaping' the spatio-temporal profile of the response...
  3. ncbi request reprint Critical role for NHE1 in intracellular pH regulation in pancreatic acinar cells
    David A Brown
    Dept of Pharmacology and Physiology, School of Medicine and Dentistry, Univ of Rochester Medical Center, 601 Elmwood Ave, Rochester, NY 14642, USA
    Am J Physiol Gastrointest Liver Physiol 285:G804-12. 2003
    ..These data demonstrate that NHE1 is the major regulator of pHi in both resting and muscarinic agonist-stimulated pancreatic acinar cells...
  4. pmc Functional inositol 1,4,5-trisphosphate receptors assembled from concatenated homo- and heteromeric subunits
    Kamil J Alzayady
    From the Department of Pharmacology and Physiology, University of Rochester, Rochester, New York 14642
    J Biol Chem 288:29772-84. 2013
    ..Importantly, the results indicate that the properties of these channels are not simply a blend of those of the constituent IP3R monomers. ..
  5. pmc ATP regulation of type-1 inositol 1,4,5-trisphosphate receptor activity does not require walker A-type ATP-binding motifs
    Matthew J Betzenhauser
    Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Biol Chem 284:16156-63. 2009
    ..Similarly, ATP increased the single channel open probability of the mutated InsP3R1 to the same extent as wild type. ATP likely exerts its effects on InsP3R1 channel function via a novel and as yet unidentified mechanism...
  6. ncbi request reprint 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...
  7. ncbi request reprint 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...
  8. ncbi request reprint 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...
  9. pmc The type 2 inositol (1,4,5)-trisphosphate (InsP3) receptor determines the sensitivity of InsP3-induced Ca2+ release to ATP in pancreatic acinar cells
    Hyung Seo Park
    Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Biol Chem 283:26081-8. 2008
    ..The effects of metabolic stress on intracellular Ca(2+) signals can therefore be determined by the relative amount of InsP(3)R2 expressed in cells...
  10. pmc Tumor necrosis factor-alpha potentiates intraneuronal Ca2+ signaling via regulation of the inositol 1,4,5-trisphosphate receptor
    KEIGAN M PARK
    Center for Neural Development and Disease, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Biol Chem 283:33069-79. 2008
    ....
  11. pmc Studying isoform-specific inositol 1,4,5-trisphosphate receptor function and regulation
    Matthew J Betzenhauser
    Department of Pharmacology and Physiology, University of Rochester, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Methods 46:177-82. 2008
    ....
  12. ncbi request reprint Functional consequences of phosphomimetic mutations at key cAMP-dependent protein kinase phosphorylation sites in the type 1 inositol 1,4,5-trisphosphate receptor
    Larry E Wagner
    Department of Pharmacology and Physiology, University of Rochester, Rochester, New York 14642, USA
    J Biol Chem 279:46242-52. 2004
    ..Thus, regulation by phosphorylation of the functional sensitivity of InsP(3)R-1 appears to define the threshold at which oscillations are initiated but not the frequency or amplitude of the signal when established...
  13. ncbi request reprint 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...
  14. pmc 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...
  15. pmc Regulation of Ca²⁺ release through inositol 1,4,5-trisphosphate receptors by adenine nucleotides in parotid acinar cells
    Hyung Seo Park
    University of Rochester Medical Center, Department of Pharmacology and Physiology, University of Rochester, Rochester, New York 14642, USA
    Am J Physiol Gastrointest Liver Physiol 302:G97-G104. 2012
    ..Adenine nucleotide modulation of InsP(3)R in parotid acinar cells likely contributes to the properties of Ca(2+) signals in physiological and pathological conditions...
  16. ncbi request reprint 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...
  17. pmc ATP modulation of Ca2+ release by type-2 and type-3 inositol (1, 4, 5)-triphosphate receptors. Differing ATP sensitivities and molecular determinants of action
    Matthew J Betzenhauser
    Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14625, USA
    J Biol Chem 283:21579-87. 2008
    ..Furthermore, this mutation had profound effects on the patterns of intracellular calcium signals, providing evidence for the physiological significance of ATP binding to InsP(3)R2...
  18. pmc Protein kinase A increases type-2 inositol 1,4,5-trisphosphate receptor activity by phosphorylation of serine 937
    Matthew J Betzenhauser
    Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Biol Chem 284:25116-25. 2009
    ..These results provide a mechanism responsible for the enhanced Ca(2+) signaling following PKA activation in cells that express predominantly InsP(3)R2...
  19. ncbi request reprint ATP binding to a unique site in the type-1 S2- inositol 1,4,5-trisphosphate receptor defines susceptibility to phosphorylation by protein kinase A
    Larry E Wagner
    Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Biol Chem 281:17410-9. 2006
    ....
  20. pmc Regulation of single inositol 1,4,5-trisphosphate receptor channel activity by protein kinase A phosphorylation
    Larry E Wagner
    Department of Pharmacology and Physiology, University of Rochester, 601 Elmwood Ave, Rochester, NY 14642, USA
    J Physiol 586:3577-96. 2008
    ....
  21. pmc Protein kinase A regulation of P2X(4) receptors: requirement for a specific motif in the C-terminus
    David A Brown
    Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY 14642, USA
    Biochim Biophys Acta 1803:275-87. 2010
    ..This may occur at least in part, by altering the trafficking of a population of P2X(4)R present at the plasma membrane...
  22. pmc InsP3R-associated cGMP kinase substrate determines inositol 1,4,5-trisphosphate receptor susceptibility to phosphoregulation by cyclic nucleotide-dependent kinases
    Wataru Masuda
    Department of Pharmacology and Physiology, University of Rochester Medical School, Rochester, New York 14642, USA
    J Biol Chem 285:37927-38. 2010
    ..These studies yield mechanistic insight into how cells with various complements of proteins integrate and prioritize signals from ubiquitous signaling pathways...
  23. ncbi request reprint 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...
  24. ncbi request reprint Phosphorylation of type-1 inositol 1,4,5-trisphosphate receptors by cyclic nucleotide-dependent protein kinases: a mutational analysis of the functionally important sites in the S2+ and S2- splice variants
    Larry E Wagner
    Department of Pharmacology and Physiology, University of Rochester, Rochester, New York 14642, USA
    J Biol Chem 278:45811-7. 2003
    ..Collectively, these data indicate that phosphoregulation of InsP3R-1 has dramatic effects on Ca2+ release and defines the molecular sites phosphorylated in the major variants expressed in neuronal and peripheral tissues...
  25. pmc Apical Ca2+-activated potassium channels in mouse parotid acinar cells
    Janos Almassy
    Department of Pharmacology and Physiology, University of Rochester Medical Center, University of Rochester, Rochester, NY 14642, USA
    J Gen Physiol 139:121-33. 2012
    ..Collectively, this study provides support for a model in which fluid secretion is optimized after expression of K channels specifically in the apical PM...
  26. pmc Protein kinase C regulation of P2X3 receptors is unlikely to involve direct receptor phosphorylation
    David A Brown
    Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Biochim Biophys Acta 1773:166-75. 2007
    ..These data indicate that PKC activation can enhance both the Ca(2+) signal as well as the cation current through P2X(3)R, however it appears that the regulation is unlikely to be a result of direct phosphorylation of the receptor...
  27. pmc Agonist activation of arachidonate-regulated Ca2+-selective (ARC) channels in murine parotid and pancreatic acinar cells
    Olivier Mignen
    Department of Pharmacology and Physiology, Box 711, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    J Physiol 564:791-801. 2005
    ..This is consistent with previous reports indicating that carbachol-induced [Ca(2+)](i) signals in these cells are much more dependent on Ca(2+) entry than are the cholecystokinin-induced responses...
  28. pmc Manganese transport via the transferrin mechanism
    Thomas E Gunter
    Department of Biochemistry and Biophysics, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Neurotoxicology 34:118-27. 2013
    ..This novel approach may prove useful for studying Mn toxicity in other systems and cell types...
  29. pmc Differential regulation of the InsP₃ receptor type-1 and -2 single channel properties by InsP₃, Ca²⁺ and ATP
    Larry E Wagner
    Department of Pharmacology, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, NY, USA
    J Physiol 590:3245-59. 2012
    ..Subtype-specific regulation of InsP3R channel activity probably contributes to the fidelity of Ca2+ signalling in cells expressing these receptor subtypes...
  30. ncbi request reprint 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...
  31. ncbi request reprint Ca2+ release dynamics in parotid and pancreatic exocrine acinar cells evoked by spatially limited flash photolysis
    Jong Hak Won
    Department of Pharmacology and Physiology, Univ of Rochester, 601 Elmwood Ave, Rochester, NY 14642, USA
    Am J Physiol Gastrointest Liver Physiol 293:G1166-77. 2007
    ..These properties may represent a specialization of the cell type to effectively stimulate Ca(2+)-dependent effectors important for the differing primary physiological role of each gland...
  32. pmc Impaired TNF-alpha control of IP3R-mediated Ca2+ release in Alzheimer's disease mouse neurons
    KEIGAN M PARK
    Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY 14642, USA
    Cell Signal 22:519-26. 2010
    ....
  33. pmc Fragmented inositol 1,4,5-trisphosphate receptors retain tetrameric architecture and form functional Ca2+ release channels
    Kamil J Alzayady
    Department of Pharmacology and Physiology, University of Rochester, Rochester, New York 14642, USA
    J Biol Chem 288:11122-34. 2013
    ..These data provide novel insights regarding the regulation of IP3R1 during proteolysis and provide direct evidence that polypeptide continuity is not required for IP3R activation and Ca(2+) release...
  34. ncbi request reprint Calcium and mitochondria
    Thomas E Gunter
    Department of Biochemistry and Biophysics, School of Medicine and Dentistry, University of Rochester, 575 Elmwood Avenue, Rochester, NY 14642, USA
    FEBS Lett 567:96-102. 2004
    ..STKE re1 (2004) 1-9], may also influence this story...
  35. ncbi request reprint Targeted phosphorylation of inositol 1,4,5-trisphosphate receptors selectively inhibits localized Ca2+ release and shapes oscillatory Ca2+ signals
    D R Giovannucci
    Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Biol Chem 275:33704-11. 2000
    ..Our data provide a simple mechanism by which distinct oscillatory Ca(2+) patterns can be shaped...
  36. pmc Tumor necrosis factor-alpha-mediated regulation of the inositol 1,4,5-trisphosphate receptor promoter
    KEIGAN M PARK
    Department of Neurology, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Biol Chem 284:27557-66. 2009
    ..Overall, these data delineate a key pathway by which TNF-alpha in a neuronal environment modulates IP(3)R expression and intracellular Ca(2+) homeostasis...
  37. ncbi request reprint Measurement of Ca2+ signaling dynamics in exocrine cells with total internal reflection microscopy
    Jong Hak Won
    Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, NY 14642, USA
    Am J Physiol Gastrointest Liver Physiol 291:G146-55. 2006
    ..In addition, TIRFM reveals that the extent of Ca2+ influx in parotid acinar cells is greater than pancreatic acinar cells when compared using identical methodologies...
  38. pmc Phenotypic changes in mouse pancreatic stellate cell Ca2+ signaling events following activation in culture and in a disease model of pancreatitis
    Jong Hak Won
    Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY 14642, USA
    Mol Biol Cell 22:421-36. 2011
    ....
  39. pmc Pancreatic acinar cells: molecular insight from studies of signal-transduction using transgenic animals
    David I Yule
    Department of Pharmacology and Physiology, University of Rochester Medical School, Rochester, NY 14642, USA david
    Int J Biochem Cell Biol 42:1757-61. 2010
    ..This brief review discusses recent studies in which transgenic animal models have been utilized to define in molecular detail the components of the Ca(2+) signaling machinery which contribute to these characteristics...
  40. pmc Respective contribution of mitochondrial superoxide and pH to mitochondria-targeted circularly permuted yellow fluorescent protein (mt-cpYFP) flash activity
    Lan Wei-Lapierre
    Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Biol Chem 288:10567-77. 2013
    ..Furthermore, flash activity depends strongly on a combination of mitochondrial oxidation and pH gradient...
  41. pmc Phospholipase Cε hydrolyzes perinuclear phosphatidylinositol 4-phosphate to regulate cardiac hypertrophy
    Lianghui Zhang
    Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Cell 153:216-27. 2013
    ....
  42. ncbi request reprint Identification of a ryanodine receptor in rat heart mitochondria
    G Beutner
    Department of Pharmacology and Physiology, University of Rochester, School of Medicine and Dentistry, Rochester, New York 14642, USA
    J Biol Chem 276:21482-8. 2001
    ..This mitochondrial ryanodine receptor is likely to play an essential role in the dynamic uptake of Ca(2+) into mitochondria during Ca(2+) oscillations...
  43. ncbi request reprint Spatiotemporal analysis of exocytosis in mouse parotid acinar cells
    Ying Chen
    Department of Neurosciences, Medical College of Ohio, Toledo, OH 43614, USA
    Am J Physiol Cell Physiol 289:C1209-19. 2005
    ..Parotid acinar cells were shown to exhibit both similar and divergent properties compared with the better-studied pancreatic acinar cell regarding spatial organization and kinetics of exocytotic fusion of zymogen granules...
  44. pmc Visualizing form and function in organotypic slices of the adult mouse parotid gland
    Jennifer D Warner
    Department of Neurosciences, Health Science Campus, The University of Toledo College of Medicine, 3035 Arlington Ave, Toledo, OH 43614, USA
    Am J Physiol Gastrointest Liver Physiol 295:G629-40. 2008
    ..This system is compatible with a variety of genetic and physiological approaches used to study secretory function...
  45. pmc A mathematical model of fluid secretion from a parotid acinar cell
    Elan Gin
    Department of Mathematics, The University of Auckland, Private Bag 92019, Auckland, New Zealand
    J Theor Biol 248:64-80. 2007
    ..We find that [Ca(2+)] oscillations lead to oscillations in fluid flow, and that the rate of fluid flow is regulated by the average calcium concentration and not the frequency of the oscillations...
  46. ncbi request reprint Akt kinase phosphorylation of inositol 1,4,5-trisphosphate receptors
    M Tariq Khan
    Department of Pathology and Cell Biology, Thomas Jefferson University School of Medicine, Philadelphia, Pennsylvania 19107, USA
    J Biol Chem 281:3731-7. 2006
    ..We conclude that IP3 receptors are in vivo substrates for Akt kinase and that phosphorylation of the IP3R may provide one mechanism to restrain the apoptotic effects of calcium...

Research Grants24

  1. Pancreatic Function: G-Protein Mediated Ca2+ Signaling
    David Yule; Fiscal Year: 2006
    ..This information is fundamentally important to appreciating the normal functioning of the gland and to the subsequent development of effective strategies for the treatment of pancreatic dysfunction. ..
  2. [Ca2+]i and Secretory Dynamics in Parotid Acinar Cells
    David Yule; Fiscal Year: 2007
    ..abstract_text> ..
  3. Pancreatic Function: G-Protein Mediated Ca2+ Signaling
    David Yule; Fiscal Year: 2007
    ..abstract_text> ..
  4. [Ca2+]i and Secretory Dynamics in Parotid Acinar Cells
    David Yule; Fiscal Year: 2009
    ..Ultimately these data are designed to lead to the design of therapeutic strategies for the treatment of xerostomia based on exploiting the physiology of remaining functional acinar tissue. ..
  5. [Ca2+]i and Secretory Dynamics in Parotid Acinar Cells
    David I Yule; Fiscal Year: 2010
    ..Ultimately these data are designed to lead to the design of therapeutic strategies for the treatment of xerostomia based on exploiting the physiology of remaining functional acinar tissue. ..
  6. Pancreatic Function: G-Protein Mediated Ca2+ Signaling
    David I Yule; Fiscal Year: 2010
    ..The long term goal of these studies is to provide a level of understanding of these processes that will ultimately aid in the design of novel therapeutic strategies for the treatment of pancreatic disease. ..
  7. Pancreatic Function: G-Protein Mediated Ca2+ Signaling
    David Yule; Fiscal Year: 2009
    ..The long term goal of these studies is to provide a level of understanding of these processes that will ultimately aid in the design of novel therapeutic strategies for the treatment of pancreatic disease. ..
  8. [Ca2+]i and Secretory Dynamics in Parotid Acinar Cells
    David Yule; Fiscal Year: 2006
    ..It is envisioned that the knowledge gained into the parotid specific mechanisms responsible for fluid and protein secretion will be important in elucidating new therapy for salivary gland dysfunction. ..
  9. PANCREATIC SECRETION--G PROTEIN MEDIATED CA++ SIGNALING
    David Yule; Fiscal Year: 2002
    ....
  10. [Ca2+]i and Secretory Dynamics in Parotid Acinar Cells
    David Yule; Fiscal Year: 2009
    ..Ultimately these data are designed to lead to the design of therapeutic strategies for the treatment of xerostomia based on exploiting the physiology of remaining functional acinar tissue. ..