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Influence of forced multimerized receptor formation on the signal transduction mechanisms

Research Project

Project/Area Number 17590469
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Applied pharmacology
Research InstitutionTakasaki University of Health and Welfare (2006)
Yamagata University (2005)

Principal Investigator

YOMOGIDA Shin-Ichi  Takasaki University of Health and Welfare, Department of Pharmacy, Associate Professor (90250802)

Co-Investigator(Kenkyū-buntansha) ENDOH Masao  Yamagata University, Vice-president (40004668)
Project Period (FY) 2005 – 2006
Project Status Completed (Fiscal Year 2006)
Budget Amount *help
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2006: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2005: ¥2,200,000 (Direct Cost: ¥2,200,000)
Keywordsendothelin / receptor / dimer
Research Abstract

In some of growth factor receptors, which involve tyrosine kinases in their molecule, it is well known that these receptors dimerize each other and ligand-induced stimulation is transduced into the cells with these dimerized receptors. Recent researches clarified that G-protein-coupled receptors, another type of the cell surface receptors also form their dimerized receptors, function as a dimer and those will regulate the intracellular signaling mechanisms.
We have researched the signal transduction mechanisms of endothelin by using rabbit heart tissue, and found that the ligand selectivity of endothelin receptors in rabbit heart is different from those reported by another species. We examined whether there are differences in molecular structure of endothelin receptors in rabbit and in other species, but the differences of the amino acid sequences of these receptors are little. Then we next examined the possibilities that endothelin receptors in rabbit heart function as dimer, and dimerized receptors-induced change in signaling mechanisms are responsible for the atypical responses for endothelin in rabbit heart tissue. There are two types of endothelin receptors named ETA and ETB, and we found both ETA and ETB receptors dimerized each other. Furthermore, it was found that these endothein receptors might form trimer, not only dimer. However, a clear result, which showed the change in intracellular mechanisms that might be induced by dimerized (or oligomerized) receptor, could not be obtained. Further analyses have been carried out to clarify the physiological and pharmacological roles of multimerized receptor in modulating the cell function.

Report

(3 results)
  • 2006 Annual Research Report   Final Research Report Summary
  • 2005 Annual Research Report
  • Research Products

    (16 results)

All 2006 2005

All Journal Article (16 results) (of which Peer Reviewed: 5 results)

  • [Journal Article] Signal transduction and Ca^<2+> signaling in intact myocardium2006

    • Author(s)
      Endoh, M.
    • Journal Title

      J. Pharmacol. Sci 100

      Pages: 525-537

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2006 Final Research Report Summary
    • Peer Reviewed
  • [Journal Article] Acute heart failure:inotropic agents and their clinical uses2006

    • Author(s)
      Endoh, M.
    • Journal Title

      Expert Opin.Pharmacother 7(16)

      Pages: 2179-2202

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2006 Final Research Report Summary
    • Peer Reviewed
  • [Journal Article] Signal transduction and Ca^<2+> signaling in intact myocardium.2006

    • Author(s)
      Endoh, M
    • Journal Title

      J. Pharmacol. Sci 100

      Pages: 525-537

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Acute heart failure : inotropic agents and their clinical uses2006

    • Author(s)
      Endoh, M
    • Journal Title

      Expert Opin. Pharmacother 7(16)

      Pages: 2179-2202

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Signal transduction and CA^<2+> signaling in intact myocardium.2006

    • Author(s)
      Endoh, M.
    • Journal Title

      J. Pharmacol. Sci. 100

      Pages: 525-537

    • Related Report
      2006 Annual Research Report
  • [Journal Article] Acute heart failure : inotropic agents and their clinical uses.2006

    • Author(s)
      Endoh, M.
    • Journal Title

      Expert Opin. Pharmacother. 7.16

      Pages: 2179-2202

    • Related Report
      2006 Annual Research Report
  • [Journal Article] Receptor subtypes mediating the inotropic effects of endothelin-1 induced by cr osstalk with norepinephrine in canine ventricular myocardium2005

    • Author(s)
      Chu L
    • Journal Title

      J. Pharmacol. Sci 97

      Pages: 417-428

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2006 Final Research Report Summary
    • Peer Reviewed
  • [Journal Article] Inhibition by the Rho kinase inhibitor Y-27632 of the increases in contractility and Ca<2+> tr ansients induced by endothelin-1 in rabbit ventricular myocytes2005

    • Author(s)
      Chu L
    • Journal Title

      Naunyn-Schmiedeberg's Arch. Pharmacol.Chu L 371

      Pages: 185-194

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2006 Final Research Report Summary
    • Peer Reviewed
  • [Journal Article] Wortmannin inhibits the myofilament Ca^<2+> sensitization induced by endot helin-12005

    • Author(s)
      Chu L
    • Journal Title

      Eur. J. Pharmacol 507

      Pages: 135-143

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2006 Final Research Report Summary
    • Peer Reviewed
  • [Journal Article] Receptor subtypes mediating the inotropic effects of endothelin-1 induced by crosstalk with norepinephrine in canine ventricular myocardium.2005

    • Author(s)
      Chu, L., et. al.
    • Journal Title

      J. Pharmacol. Sci. 97

      Pages: 417-428

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Inhibition by the Rho kinase inhibitor Y-27632 of the increases in contractility and Ca^<2+> transients induced by endothelin-1 in rabbit ventricular myocytes.2005

    • Author(s)
      Chu, L., et. al.
    • Journal Title

      Naunyn-Schmiedeberg's Arch. Pharmacol 371

      Pages: 185-194

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Wortmannin inhibits the myofilament Ca^<2+> sensitization induced by endothelin-1.2005

    • Author(s)
      Chu, L., et. al.
    • Journal Title

      Eur. J. Pharmacol 507

      Pages: 135-143

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Receptor subtypes mediating the inotropic effects of endothelin-1 induced by crosstalk with norepinephrine in canine ventricular myocardium.2005

    • Author(s)
      Chu L
    • Journal Title

      J Pharmacol Sci 97

      Pages: 417-428

    • Related Report
      2005 Annual Research Report
  • [Journal Article] Inhibition by the Rho kinase inhibitor Y-27632 of the increases in contractility and Ca^<2+> transients induced by endothelin-l in rabbit ventricular myocytes.2005

    • Author(s)
      Chu L
    • Journal Title

      Naunyn-Schmiedeberg's Arch Pharmacol 371

      Pages: 185-194

    • Related Report
      2005 Annual Research Report
  • [Journal Article] Wortmannin inhibits the myofilament Ca^<2+> sensitization induced by endothelin-1.2005

    • Author(s)
      Chu L
    • Journal Title

      Eur J Pharmacol 507

      Pages: 135-143

    • Related Report
      2005 Annual Research Report
  • [Journal Article] Differential action of a protein tyrosine kinase inhibitor, genistein, on the positive inotropic effect of endothelin-1 and norepinephrine in canine ventricular myocardium.2005

    • Author(s)
      Chu L
    • Journal Title

      Br J Pharmacol 144

      Pages: 430-442

    • Related Report
      2005 Annual Research Report

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Published: 2005-04-01   Modified: 2016-04-21  

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