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].


Hydrolysis Albumin Electrophoresis MgCl Acetylcholine 


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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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