Skip to main content

The Inositide and Arachidonic Acid Signal System

  • Chapter
Control of the Thyroid Gland

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 261))

Abstract

The concept that inositol phospholipid hydrolysis is a very early event and is responsible for transducing the effect of hormone-receptor stimulation to the cell interior is now widely accepted. The activation of these specific receptors stimulates phospholipase C which degrades membrane-bound phosphatidylinositol 4,5-bisphosphate to produce two second messengers: inositol 1,4,5-trisphosphate, which can liberate Ca2+ from intracellular stores, and 1,2-diacylglycerol, which activates protein kinase C. The membrane-bound transducer that relates the message from the receptor to the phospholipase C seems to be a specific GTP-binding protein, that is referred to as Gp, where p stands for phosphoinositide.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 84.99
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 109.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. M.J. Berridge, Inositol trisphosphate and diacylglycerol: two interacting secondary messengers. Annu. Rev. Biochem., 56: 159 - 193 (1987).

    Article  PubMed  CAS  Google Scholar 

  2. Y. Nishizuka, The role of protein kinase C in cell surface signal transduction and tumour promotion. Nature, 308: 693 - 698 (1984).

    Article  PubMed  CAS  Google Scholar 

  3. S. Cockcroft and B.D. Gomperts, Role of guanine nucleotide binding protein in the activation of polyphosphoinositide phosphodiesterase. Nature, 314: 534 - 536 (1985).

    Article  PubMed  CAS  Google Scholar 

  4. I. Litosch and J.N. Fain, Regulation of phosphoinositide breakdown by guanine nucleotides. Life Sci. 39: 187 - 194 (1986).

    Article  PubMed  CAS  Google Scholar 

  5. E.G. Lapetina, Inositide-dependent and independent mechanisms in platelet activation. In: Phosphoinositides and Receptor Mechanisms, edited by J.W. Putney, Jr., p. 271. Alan R. Liss, New York (1986).

    Google Scholar 

  6. E.G. Lapetina, Regulation of arachidonic acid production: Role of phospholipases C and A2, Trends in Pharmacol. Sci. 3: 115 - 118, (1982).

    CAS  Google Scholar 

  7. M.F. Crouch and E.G. Lapetina, No direct correlation between Ca2+ mobilization and dissociation of Gi during phospholipase A2 activation. Biochem. Biophys. Res. Commun. 153: 21 - 30 (1988).

    Article  PubMed  CAS  Google Scholar 

  8. M.M. Billah and E.G. Lapetina, Rapid decrease of phosphatidylinositol 4,5-bisphosphate in thrombin-stimulated platelets. J. Biol. Chem., 257: 12705 - 12708 (1982).

    PubMed  CAS  Google Scholar 

  9. S. Rittenhouse-Simmons, Production of diglyceride from phosphatidylinositol in activated human platelets. J. Clin. Invest., 63: 580 - 587 (1979).

    Article  PubMed  CAS  Google Scholar 

  10. P.W. Majerus, D.B. Wilson, T.M. Connolly, T.E. Bross and E.J. Neufeld, Phosphoinositide turnover provides a link in stimulus-response coupling. TIBS. 10: 168 - 171 (1985).

    CAS  Google Scholar 

  11. H. Streb, R.F. Irvine, M.J. Berridge and I. Schulz, Release of Ca2+ from a nonmitochondrial intracellular store in pancreatic acinar cells by inositol-1,4,5-trisphosphate. Nature, 306: 67 - 69 (1983).

    Article  PubMed  CAS  Google Scholar 

  12. L. Molina y Vedia and E.G. Lapetina, Phorbol 12,13-dibutyrate and 1-oleyl, 2-acetyl-diacylglycerol stimulate inositol trisphosphate dephosphorylation in human platelets. J. Biol. Chem. 261: 10493 - 10495 (1986).

    Google Scholar 

  13. L. Molina y Vedia and E.G. Lapetina, Subcellular localization of the enzymes that dephosphorylate myoinositol phosphates in human platelets. Biochem. J. 255: 795 - 800 (1988).

    Google Scholar 

  14. T.M. Connolly, T.E. Bross and P.W. Majerus, Isolation of a phosphomonoesterase from human platelets that specifically hydrolyses the 5-phosphate of inositol 1,4,5-trisphosphate. J. Biol. Chem., 260: 7868 - 7874 (1985).

    PubMed  CAS  Google Scholar 

  15. R.F. Irvine, A.J. Letcher, J.P. Heslop and M.J. Berridge,The inositol tris/tetrakisphosphate pathway: demonstration of Ins (1,4,5) P3 3-kinase activity in animal tissues. Nature, 320: 631 - 634 (1986).

    Article  PubMed  CAS  Google Scholar 

  16. T.J. Giden, M. Comte, J.A. Cox and C.B. Wollheim, Calcium calmodulin stimulates inositol 1,4,5-trisphosphate kinase activity from insulin-secreting RINm 5F cells. J. Biol. Chem., 262: 9437 - 9440 (1987).

    Google Scholar 

  17. A.E. Traynor-Kaplan, A.L. Harris, B.L. Thompson, P. Taylor and L.A. Sklar, An inositol tetrakisphosphate-containing phospholipid in activated neutrophils. Nature 334:353 - 356 (1988).

    Article  PubMed  CAS  Google Scholar 

  18. M. Whitman, C.P. Downes, M. Keeler, T. Keller and L. Cantley, Type I phosphatidylinositol kinase makes a novel inositol phospholipid, phosphatidylinositol-3-phosphate. Nature 332:644 - 646 (1988).

    Article  PubMed  CAS  Google Scholar 

  19. T. Balla, G. Guillemette, A.J. Baukal and K.J. Catt, Metabolism of inositol 1,3,4-trisphosphate to a new tetrakisphosphate isomer in angiotensin-stimulated adrenal glomerulosa cells. J. Biol. Chem. 262: 9952 - 9955 (1987).

    PubMed  CAS  Google Scholar 

  20. M.F. Crouch and E.G. Lapetina, A role for Gi in control of thrombin receptor-phospholipase C coupling in human platelets. J. Biol Chem., 263: 3363 - 3371 (1988).

    PubMed  CAS  Google Scholar 

  21. E.G. Lapetina, J.C. Lacal, B.R. Reep and L. Molina y Vedia, A ras-related protein is phosphorylated and translocated by agonists that increase cyclic AMP levels in human platelets, Proc. Natl. Acad. Sei. U.S.A. 86: 3131 - 3134 (1989).

    Article  CAS  Google Scholar 

  22. S.P. Watson, R.T. McConnell and E.G. Lapetina, The rapid formation of inositol phosphates in human platelets by thrombin is inhibited by prostacyclin. J. Biol. Chem., 259: 13199 - 13203 (1984).

    PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 1989 Springer Science+Business Media New York

About this chapter

Cite this chapter

Lapetina, E.G. (1989). The Inositide and Arachidonic Acid Signal System. In: Ekholm, R., Kohn, L.D., Wollman, S.H. (eds) Control of the Thyroid Gland. Advances in Experimental Medicine and Biology, vol 261. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-2058-7_11

Download citation

  • DOI: https://doi.org/10.1007/978-1-4757-2058-7_11

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4757-2060-0

  • Online ISBN: 978-1-4757-2058-7

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics