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The Journal of Immunology, 2008, 181, 4441 -4445
Copyright © 2008 by The American Association of Immunologists, Inc.
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Transcriptional Outcome of Wnt-Frizzled Signal Transduction in Inflammation: Evolving Concepts

Malini Sen*,1 and Gourisankar Ghosh{dagger}

* Division of Infectious Diseases and Immunology, Indian Institute of Chemical Biology, Kolkata, India; and {dagger} Department of Chemistry and Biochemistry, University of California, San Diego; La Jolla, CA 92093

Wnt-Frizzled signaling was first identified as a key event in Drosophila development. Over the years, ample evidence has accumulated regarding the multiple roles of Wnt-Frizzled signaling in mammalian cell differentiation and tissue/organ morphogenesis. It is thus not surprising that variations in the regulatory network of the Wnt signaling scheme would lead to alterations in cellular organization and cell activation and to the development of pathogenic conditions. Several reports have accordingly implied the involvement of Wnt-Frizzled signaling in the activation of proinflammatory mediators in inflammatory disorders. We will discuss how Wnt-Frizzled signaling may initiate/augment inflammation, focusing on its transcriptional outcome.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

1 Address correspondence and reprint requests to Dr. Malini Sen, Division of Infectious Diseases and Immunology, Indian Institute of Chemical Biology, 4 Raja S. C. Mallick Road, Kolkata 700032, India. E-mail address: msen{at}iicb.res.in

2 Abbreviations used in this paper: Fz, Frizzled; CaMK, calmodulin kinase; Dv, Disheveled; GSK3β, glycogen synthase kinase 3b; LEF, lymphoid enhancing factor; PKC, protein kinase C; PLC, phospholipase C; RA, rheumatoid arthritis; ROR, retinoic acid-related orphan receptor; TCF, T cell factor.






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