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• W2036007568 abstract "The α(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." @default.
• W2036007568 created "2016-06-24" @default.
• W2036007568 creator A5021888249 @default.
• W2036007568 creator A5026755902 @default.
• W2036007568 date "2004-09-01" @default.
• W2036007568 modified "2023-09-26" @default.
• W2036007568 title "H-Ras and Phosphoinositide 3-Kinase Cooperate to Induce α(1,3)-Fucosyltransferase VII Expression in Jurkat T Cells" @default.
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• W2036007568 doi "https://doi.org/10.1074/jbc.m407904200" @default.
• W2036007568 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15262995" @default.
• W2036007568 hasPublicationYear "2004" @default.
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