Arachidonic acid, a principal product of Rac-activated phospholipase A2, stimulates c-fos serum response element via Rho-dependent mechanism

Byung Chul Kim, Chang Jin Lim, Jae Hong Kim

Research output: Contribution to journalArticlepeer-review

26 Citations (Scopus)

Abstract

Previously, we have reported that phospholipase A2 (PLA2) is one of the major downstream targets by which Rac GTPase mediates the activation of c-fos serum response element (SRE) in response to agonists such as EGF [FEBS Lett. 407 (1997) 7-12]. Thus, the potential activity of arachidonic acid (AA), a principal product of Rac-activated PLA2, on c-fos SRE stimulation has been suggested. Here, we provide evidence about the biological activity of AA on c-fos SRE activation. Further, we observed that co-transfection with expression plasmid of either RhoN19, a dominant negative RhoA mutant, or botulinum C3 transferase which inhibits Rho via ADP ribosylation, selectively repressed AA- or Rac-induced SRE activation, suggesting that Rho activity is critical for the signaling cascade of 'Rac-PLA2-AA' to c-fos SRE. Thus, Rac signaling to the nucleus appears to be, at least partly, mediated by a Rho-linked pathway and this Rat-Rho signaling connection is mediated by AA, In accordance with the role of Rho as a potential mediator of AA signaling to the nucleus, AA induces a rapid translocation of RhoA.

Original languageEnglish
Pages (from-to)325-328
Number of pages4
JournalFEBS Letters
Volume415
Issue number3
DOIs
Publication statusPublished - 1997 Oct 6
Externally publishedYes

Bibliographical note

Funding Information:
This study was supported by the Korean Ministry of Education through Research Fund, 1996 (to J.H. Kim). We wish to thank Dr. Richard Treisman (Imperial Cancer Research Fund Laboratory, London, UK) for providing EF and EF-C3 plasmids.

Keywords

  • Arachidonic acid
  • Phospholipase A
  • Rac
  • Rho
  • c-fos serum response element

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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