Intestinal Secretory Defects and Dwarfism in Mice Lacking cGMP-Dependent Protein Kinase II

DOI Web Site 被引用文献22件
  • Alexander Pfeifer
    A. Pfeifer, P. Ruth, F. Hofmann, Institut für Pharmakologie und Toxikologie, Technische Universität München, Biedersteiner Strasse 29, D-80802 München, Germany.
  • Attila Aszódi
    A. Aszódi and R. Fässler, Max-Planck-Institut für Biochemie, D-82152 Martinsried, Germany.
  • Ursula Seidler
    U. Seidler, Medizinische Klinik I, Eberhard-Karls-Universität Tübingen, D-72076 Tübingen, Germany.
  • Peter Ruth
    A. Pfeifer, P. Ruth, F. Hofmann, Institut für Pharmakologie und Toxikologie, Technische Universität München, Biedersteiner Strasse 29, D-80802 München, Germany.
  • Franz Hofmann
    A. Pfeifer, P. Ruth, F. Hofmann, Institut für Pharmakologie und Toxikologie, Technische Universität München, Biedersteiner Strasse 29, D-80802 München, Germany.
  • Reinhard Fässler
    A. Aszódi and R. Fässler, Max-Planck-Institut für Biochemie, D-82152 Martinsried, Germany.

抄録

<jats:p> Cyclic guanosine 3′,5′-monophosphate (cGMP)-dependent protein kinases (cGKs) mediate cellular signaling induced by nitric oxide and cGMP. Mice deficient in the type II cGK were resistant to <jats:italic>Escherichia coli</jats:italic> STa, an enterotoxin that stimulates cGMP accumulation and intestinal fluid secretion. The cGKII-deficient mice also developed dwarfism that was caused by a severe defect in endochondral ossification at the growth plates. These results indicate that cGKII plays a central role in diverse physiological processes. </jats:p>

収録刊行物

  • Science

    Science 274 (5295), 2082-2086, 1996-12-20

    American Association for the Advancement of Science (AAAS)

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