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J. Biol. Chem., Vol. 279, Issue 38, 39495-39504, September 17, 2004

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H-Ras and Phosphoinositide 3-Kinase Cooperate to Induce (1,3)-Fucosyltransferase VII Expression in Jurkat T Cells^*

Dimitrios G. Zisoulis and Geoffrey S. Kansas

From the Department of Microbiology-Immunology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611

The (1,3)-fucosyltransferase FucT-VII is essential for the biosynthesis of selectin ligands, but the signaling pathways mediating FucT-VII induction in T cells and other lymphocytes are poorly understood. We have shown previously that sustained activation of Ras in Jurkat T cells induces FucT-VII transcription, which requires the Raf-MEK-ERK pathway. In this study we report that FucT-VII induction is specific to the H-Ras isoform. Jurkat T cells retrovirally transduced with constitutively active H-Ras but not N- or K-Ras up-regulated expression of FucT-VII. Pharmacological inhibition studies also revealed that phosphoinositide 3-kinase (PI3K) activity is required for H-Ras-mediated FucT-VII induction. However, the ability of H-Ras to selectively induce FucT-VII is not a function of the inability of the N- or K-Ras isoforms to activate Raf or PI3K pathways. The use of effector-loop domain mutants of H-Ras, which are impaired for their ability to interact selectively with individual effectors alone or in combination with active Raf, indicated that induction of FucT-VII requires the concomitant activation of at least three signaling pathways. These studies show that H-Ras mediates FucT-VII induction in Jurkat T cells via the activation of the Raf, PI3K, and a distinct, H-Ras-specific effector signaling pathway.

Received for publication, July 13, 2004

^* This work was supported by National Institutes of Health Grant AI50837 (to G. S. K.) and American Heart Association Pre-doctoral Fellowship 0410069Z (to D. G. Z.). 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.

To whom correspondence should be addressed: Dept. of Microbiology-Immunology, Northwestern Medical School, 303 E. Chicago Ave., Chicago, IL 60611. Tel.: 312-908-3237; Fax: 312-503-1339; E-mail: gsk{at}northwestern.edu.

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