Calcium Signaling Regulates Translocation and Activation of Rac*

  1. John G. Collard
  1. Division of Cell Biology, The Netherlands Cancer Institute, Plesmanlaan 121, Amsterdam 1066 CX, The Netherlands and Department of Experimental Immunohematology, Sanquin Research at CLB, Plesmanlaan 125, Amsterdam 1066 CX, The Netherlands
  1. To whom correspondence should be addressed. Tel.: 31-20-512-1932; Fax: 31-20-512-1944; E-mail: j.collard{at}nki.nl.

Abstract

Rac is activated in response to various stimuli including growth factors and by adhesion to the extracellular matrix. However, how these stimuli ultimately result in Rac activation is poorly understood. The increase in intracellular calcium [Ca2+]i represents a ubiquitous second messenger system in cells, linking receptor activation to downstream signaling pathways. Here we show that elevation of [Ca2+]i, either artificially or by thrombin receptor activation, potently induces Rac activation. Lamellipodia formation induced by artificial elevation of [Ca2+]i is blocked by inhibition of Rac signaling, indicating that calcium-induced cytoskeletal changes are controlled by the activation of Rac. Calcium-dependent Rac activation was dependent on the activation of a conventional protein kinase C. Furthermore, both increased [Ca2+]i and protein kinase C activation induce phosphorylation of RhoGDIα and induce the translocation of cytosolic Rac to the plasma membrane. Intracellular calcium signaling may thus contribute to the intracellular localization and activation of Rac to regulate the cytoskeletal changes in response to receptor stimulation.

  • Received February 27, 2003.
  • Revision received July 18, 2003.
Table of Contents

This Article

  1. The Journal of Biological Chemistry 278, 39413-39421.
  1. All Versions of this Article:
    1. M302083200v1
    2. 278/41/39413 (most recent)

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