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pubmed-article:11698498pubmed:abstractTextNormal human basophils express the integrin, VLA-4, and cross-linking their high-affinity IgE receptor, FcepsilonRI, increases their VLA-4-dependent adhesion to VCAM-1-transfected Chinese hamster ovary (CHO) cells. Here we show that the FcepsilonRI-mediated up-regulation of normal basophil VLA-4 adhesion is abolished by the Src inhibitor, PP1, the Syk inhibitor, ER-27319, and the phosphatidylinositol 3-kinase inhibitor, wortmannin. PP1, but not ER-27319 or wortmannin, also reduces basal adhesion and adhesion stimulated by chemotactic peptide, by Ca(++) ionophores, and by phorbol myristate acetate (PMA). Nonreleaser basophils (the consistently Syk-deficient, variably Lyn-deficient, severely degranulation-impaired cells found in about 10% of donors) share the PP1 phenotype of lowered basal adhesion, no FcepsilonRI-mediated adhesion up-regulation, and reduced adhesive responses to chemoattractant ionophores and PMA. These results implicate Src kinases in the control of basal VLA-4 activity and place Syk and phosphatidylinositol 3-kinase in the pathway linking FcepsilonRI cross-linking to VLA-4 up-regulation. Both Src and Syk-regulated components of adhesion may be impaired in nonreleaser basophils.lld:pubmed
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pubmed-article:11698498pubmed:authorpubmed-author:OliverJ MJMlld:pubmed
pubmed-article:11698498pubmed:authorpubmed-author:WilsonB SBSlld:pubmed
pubmed-article:11698498pubmed:authorpubmed-author:AndrewsR PRPlld:pubmed
pubmed-article:11698498pubmed:authorpubmed-author:YoussefLLlld:pubmed
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pubmed-article:11698498pubmed:dateRevised2011-11-2lld:pubmed
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pubmed-article:11698498pubmed:articleTitleRegulation of the very late antigen-4-mediated adhesive activity of normal and nonreleaser basophils: roles for Src, Syk, and phosphatidylinositol 3-kinase.lld:pubmed
pubmed-article:11698498pubmed:affiliationDepartment of Pathology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA. randrews@salud.unm.edulld:pubmed
pubmed-article:11698498pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11698498pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed