G G Holz

Summary

Affiliation: New York University
Country: USA

Publications

  1. pmc Cell physiology of cAMP sensor Epac
    George G Holz
    Department of Physiology and Neuroscience, New York University School of Medicine, New York, NY 10016, USA
    J Physiol 577:5-15. 2006
  2. pmc Epac-selective cAMP analogs: new tools with which to evaluate the signal transduction properties of cAMP-regulated guanine nucleotide exchange factors
    George G Holz
    Department of Physiology and Neuroscience, New York University School of Medicine, New York, NY, USA
    Cell Signal 20:10-20. 2008
  3. pmc A cAMP and Ca2+ coincidence detector in support of Ca2+-induced Ca2+ release in mouse pancreatic beta cells
    Guoxin Kang
    Department of Physiology and Neuroscience, New York University School of Medicine, New York, NY 10016, USA
    J Physiol 566:173-88. 2005
  4. pmc Insulinotropic toxins as molecular probes for analysis of glucagon-likepeptide-1 receptor-mediated signal transduction in pancreatic beta-cells
    G G Holz
    Department of Physiology and Neuroscience, Medical Sciences Building Room 442, New York University School of Medicine, 550 First Avenue, NY New York 10016, USA
    Biochimie 82:915-26. 2000
  5. pmc Diabetes outfoxed by GLP-1?
    George G Holz
    Department of Physiology and Neuroscience, New York University School of Medicine, New York, NY 10016, USA
    Sci STKE 2005:pe2. 2005
  6. pmc New insights concerning the glucose-dependent insulin secretagogue action of glucagon-like peptide-1 in pancreatic beta-cells
    G G Holz
    Department of Physiology and Neuroscience, New York University School of Medicine, NY 10016, USA
    Horm Metab Res 36:787-94. 2004
  7. pmc Glucagon-like peptide-1 synthetic analogs: new therapeutic agents for use in the treatment of diabetes mellitus
    George G Holz
    Department of Physiology and Neuroscience, New York University School of Medicine, New York, 10016, USA
    Curr Med Chem 10:2471-83. 2003
  8. pmc cAMP-regulated guanine nucleotide exchange factor II (Epac2) mediates Ca2+-induced Ca2+ release in INS-1 pancreatic beta-cells
    G Kang
    Department of Physiology and Neuroscience, New York University School of Medicine, New York, NY 10016, USA
    J Physiol 536:375-85. 2001
  9. pmc Over-expression of the glucagon-like peptide-1 receptor on INS-1 cells confers autocrine stimulation of insulin gene promoter activity: a strategy for production of pancreatic beta-cell lines for use in transplantation
    Oleg G Chepurny
    Department of Physiology and Neuroscience, New York University School of Medicine, New York, NY 10016, USA
    Cell Tissue Res 307:191-201. 2002
  10. pmc Epac: A new cAMP-binding protein in support of glucagon-like peptide-1 receptor-mediated signal transduction in the pancreatic beta-cell
    George G Holz
    Department of Physiology and Neuroscience, New York University School of Medicine, New York, New York 10016, USA
    Diabetes 53:5-13. 2004

Research Grants

Collaborators

Detail Information

Publications22

  1. pmc Cell physiology of cAMP sensor Epac
    George G Holz
    Department of Physiology and Neuroscience, New York University School of Medicine, New York, NY 10016, USA
    J Physiol 577:5-15. 2006
    ..Emphasized is the emerging role of Epac in the cAMP-dependent regulation of ion channel function, intracellular Ca(2+) signalling, ion transporter activity and exocytosis...
  2. pmc Epac-selective cAMP analogs: new tools with which to evaluate the signal transduction properties of cAMP-regulated guanine nucleotide exchange factors
    George G Holz
    Department of Physiology and Neuroscience, New York University School of Medicine, New York, NY, USA
    Cell Signal 20:10-20. 2008
    ..Also emphasized is the usefulness of ESCAs as new tools with which to assess the role of Epac as a determinant of intracellular Ca2+ signalling, ion channel function, neurotransmitter release, and hormone secretion...
  3. pmc A cAMP and Ca2+ coincidence detector in support of Ca2+-induced Ca2+ release in mouse pancreatic beta cells
    Guoxin Kang
    Department of Physiology and Neuroscience, New York University School of Medicine, New York, NY 10016, USA
    J Physiol 566:173-88. 2005
    ..We propose that second messenger coincidence detection of this type may explain how GLP-1 interacts with beta cell glucose metabolism to stimulate insulin secretion...
  4. pmc Insulinotropic toxins as molecular probes for analysis of glucagon-likepeptide-1 receptor-mediated signal transduction in pancreatic beta-cells
    G G Holz
    Department of Physiology and Neuroscience, Medical Sciences Building Room 442, New York University School of Medicine, 550 First Avenue, NY New York 10016, USA
    Biochimie 82:915-26. 2000
    ....
  5. pmc Diabetes outfoxed by GLP-1?
    George G Holz
    Department of Physiology and Neuroscience, New York University School of Medicine, New York, NY 10016, USA
    Sci STKE 2005:pe2. 2005
    ..This STKE Perspective summarizes signaling properties of GLP-1 that may explain its ability to increase beta-cell mass, to increase pancreatic insulin secretory capacity, and to lower levels of blood glucose in type 2 diabetic subjects...
  6. pmc New insights concerning the glucose-dependent insulin secretagogue action of glucagon-like peptide-1 in pancreatic beta-cells
    G G Holz
    Department of Physiology and Neuroscience, New York University School of Medicine, NY 10016, USA
    Horm Metab Res 36:787-94. 2004
    ..This new "feed-forward" hypothesis of beta-cell stimulus-secretion coupling may provide a mechanistic explanation as to how GLP-1 exerts a beneficial blood glucose-lowering effect in type 2 diabetic subjects...
  7. pmc Glucagon-like peptide-1 synthetic analogs: new therapeutic agents for use in the treatment of diabetes mellitus
    George G Holz
    Department of Physiology and Neuroscience, New York University School of Medicine, New York, 10016, USA
    Curr Med Chem 10:2471-83. 2003
    ..The usefulness of synthetic GLP-1 analogs as blood glucose-lowering agents is discussed, and the applicability of GLP-1 as a therapeutic agent for treatment of type 2 diabetes is highlighted...
  8. pmc cAMP-regulated guanine nucleotide exchange factor II (Epac2) mediates Ca2+-induced Ca2+ release in INS-1 pancreatic beta-cells
    G Kang
    Department of Physiology and Neuroscience, New York University School of Medicine, New York, NY 10016, USA
    J Physiol 536:375-85. 2001
    ..6. It is concluded that CICR in INS-1 cells results from GLP-1 receptor-mediated sensitization of the intracellular Ca2+ release mechanism, a signal transduction pathway independent of PKA, but which requires cAMP-GEF-II...
  9. pmc Over-expression of the glucagon-like peptide-1 receptor on INS-1 cells confers autocrine stimulation of insulin gene promoter activity: a strategy for production of pancreatic beta-cell lines for use in transplantation
    Oleg G Chepurny
    Department of Physiology and Neuroscience, New York University School of Medicine, New York, NY 10016, USA
    Cell Tissue Res 307:191-201. 2002
    ....
  10. pmc Epac: A new cAMP-binding protein in support of glucagon-like peptide-1 receptor-mediated signal transduction in the pancreatic beta-cell
    George G Holz
    Department of Physiology and Neuroscience, New York University School of Medicine, New York, New York 10016, USA
    Diabetes 53:5-13. 2004
    ..This article summarizes new findings concerning GLP-1 receptor-mediated signal transduction and seeks to define the relative importance of Epac and PKA to beta-cell stimulus-secretion coupling...
  11. pmc Epac-selective cAMP analog 8-pCPT-2'-O-Me-cAMP as a stimulus for Ca2+-induced Ca2+ release and exocytosis in pancreatic beta-cells
    Guoxin Kang
    Department of Physiology and Neuroscience, New York University School of Medicine, New York 10016, USA
    J Biol Chem 278:8279-85. 2003
    ....
  12. pmc Exendin-4 as a stimulator of rat insulin I gene promoter activity via bZIP/CRE interactions sensitive to serine/threonine protein kinase inhibitor Ro 31-8220
    Oleg G Chepurny
    Department of Physiology, New York University School of Medicine, New York, New York 10016, USA
    Endocrinology 143:2303-13. 2002
    ..It is concluded that the bZIP and CRE-mediated stimulation of RIP1 by Ex-4 explains, at least in part, how this insulinotropic hormone facilitates transcriptional activity of the rat insulin I gene...
  13. pmc Amplification of exocytosis by Ca2+-induced Ca2+ release in INS-1 pancreatic beta cells
    Guoxin Kang
    Department of Physiology and Neuroscience, New York University School of Medicine, New York, NY 10016, USA
    J Physiol 546:175-89. 2003
    ..The transition from NS-type to S-type exocytosis may represent an amplification mechanism for Ca(2+)-dependent exocytosis...
  14. pmc Role of the cAMP sensor Epac as a determinant of KATP channel ATP sensitivity in human pancreatic beta-cells and rat INS-1 cells
    Guoxin Kang
    Department of Physiology, New York University School of Medicine, New York, NY, USA
    J Physiol 586:1307-19. 2008
    ..On the basis of such findings it is concluded that there exists in human beta-cells and rat INS-1 cells a novel form of ion channel modulation in which the ATP sensitivity of K(ATP) channels is regulated by Epac...
  15. pmc cAMP sensor Epac as a determinant of ATP-sensitive potassium channel activity in human pancreatic beta cells and rat INS-1 cells
    Guoxin Kang
    Department of Physiology and Neuroscience, New York University School of Medicine, New York, NY, USA
    J Physiol 573:595-609. 2006
    ....
  16. pmc A novel cyclic adenosine monophosphate responsive luciferase reporter incorporating a nonpalindromic cyclic adenosine monophosphate response element provides optimal performance for use in G protein coupled receptor drug discovery efforts
    Oleg G Chepurny
    Department of Physiology and Neuroscience, New York University School of Medicine, New York, New York, USA
    J Biomol Screen 12:740-6. 2007
    ....
  17. pmc In vivo derivation of glucose-competent pancreatic endocrine cells from bone marrow without evidence of cell fusion
    Andreea Ianus
    Department of Pathology, New York University School of Medicine, New York, New York 10016, USA
    J Clin Invest 111:843-50. 2003
    ..The results generated with the CRE-LoxP system also suggest that in vivo cell fusion is an unlikely explanation for the "transdifferentiation" of bone marrow-derived cells into differentiated cell phenotypes...
  18. pmc Simultaneous optical measurements of cytosolic Ca2+ and cAMP in single cells
    Mark C Harbeck
    Department of Medicine, The University of Chicago, Chicago, IL 60637, USA
    Sci STKE 2006:pl6. 2006
    ..This real-time imaging method allows investigation of the dynamic organization and integration of multiple levels of signal processing in single living cells...
  19. pmc Interplay of Ca2+ and cAMP signaling in the insulin-secreting MIN6 beta-cell line
    Luis R Landa
    Department of Medicine, The University of Chicago, Chicago, Illinois 60637, USA
    J Biol Chem 280:31294-302. 2005
    ....
  20. pmc Synchronizing Ca2+ and cAMP oscillations in pancreatic beta-cells: a role for glucose metabolism and GLP-1 receptors? Focus on "regulation of cAMP dynamics by Ca2+ and G protein-coupled receptors in the pancreatic beta-cell: a computational approach&
    George G Holz
    Am J Physiol Cell Physiol 294:C4-6. 2008
  21. pmc Glucagon-like peptide-1 mobilizes intracellular Ca2+ and stimulates mitochondrial ATP synthesis in pancreatic MIN6 beta-cells
    Takashi Tsuboi
    Henry Wellcome Laboratories for Integrated Cell Signalling, Department of Biochemistry, School of Medical Sciences, University of Bristol, University Walk, Bristol BS8 1TD, U K
    Biochem J 369:287-99. 2003
    ..Taken together, these results demonstrate that GLP-1 potentiates glucose-stimulated insulin release in part via the mobilization of intracellular Ca(2+), and the stimulation of mitochondrial ATP synthesis...
  22. pmc Cytosolic adenylate kinases regulate K-ATP channel activity in human beta-cells
    Violeta Stanojevic
    Laboratory of Molecular Endocrinology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA
    Biochem Biophys Res Commun 368:614-9. 2008
    ..The down-regulation of AK1 expression by hyperglycemia may contribute to the defective coupling of glucose metabolism to K-ATP channel activity in type 2 diabetes...

Research Grants1

  1. MOLECULAR BASIS OF ANTIDIABETOGENIC HORMONE ACTION
    GEORGE HOLZ; Fiscal Year: 2007
    ..We wish to establish the molecular basis for "antidiabetogenic" properties of a new class of blood glucose-lowering agents that activate the GLP-1-R and which stimulate pancreatic insulin secretion. ..