Regulation of Signal Transduction by G Proteins in Exocrine Pancreas Cells

  • I. Schulz
  • S. Schnefel
  • R. Schäfer
Conference paper
Part of the Bayer AG Centenary Symposium book series (BAYER)


The second messenger for hormone-induced Ca2+ release is inositol 1,4,5-triphosph ate (IP3) [14]. Following binding of an agonist to its receptor, phospholipase C (PLC) is activated and phosphatidylinositoI4,5-bisphosphate is broken down to IP3 and diacylglycerol (Fig. 1). While IP3 releases Ca2+ from a nonmitochondrial compartment, which is most likely the endoplasmatic reticulum [15], diacylglycerol activates protein kinase C which in many cells leads to the final cell response by kinase C mediated phosphorylation of target proteins [9]. IP3 can be metabolized by dephosphorylation to inositol 1,4-bisphosphate (IP2) or by phosphorylation to inositol 1,3,4,5-tetrakisphosphate (IP4), which is supposed to be involved in Ca2+ influx into the cell, the mechanism of which is yet not quite clear. The two molecules IP4 and IP3 seem to act together to control Ca2+ influx [5, 8]. A current model is based on the hypothesis that Ca2+ enters the cell through an IP3-sensitive Ca2+ pool in a manner similar to that proposed by Putney [10, 11], and that IP3 modulates Ca2+ entry into that Ca2+ store [8]. Thus, the Ca2+ pool can be filled from the outside of the cell, and Ca2+ influx takes place only if the pool is emptied due to IPrinduced Ca2+ release. IP4 is dephosphorylated to inositol 1,3,4-trisphosphate of which a second messenger function is not yet known. Evidence suggests that in receptor-mediated activation of PLC GTP-binding proteins (G proteins) are involved [3].


Acinar Cell Cholera Toxin Vasoactive Intestinal Polypeptide Pertussis Toxin Pancreatic Acinar Cell 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


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Copyright information

© Springer-Verlag Berlin Heidelberg 1988

Authors and Affiliations

  • I. Schulz
    • 1
  • S. Schnefel
    • 1
  • R. Schäfer
    • 1
  1. 1.Max-Planck-Institut für BiophysikFrankfurt am Main 70Germany

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