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pubmed-article:9341768pubmed:abstractTextWe recently showed, using human Jurkat T cell variants lacking the T cell receptor (TCR)/CD3 complex, that the lectin jacalin is able to trigger intracellular calcium increase provided that CD4 is expressed on the cell surface. Involvement of the CD4 molecule in jacalin-induced biological effects was furthermore demonstrated in differentiated U937 myelomonocytic cells expressing or not expressing CD4, and is confirmed here in human CD4-transfected mouse thymoma cells. In the present paper, we analyze the CD4-associated calcium response triggered by jacalin independently of the TCR/CD3 complex. We show that the observed calcium rise results from a direct long-lasting calcium influx from the outside without release of calcium from intracellular stores. We demonstrate that it is independent of the phosphoinositide phospholipase C transduction pathway. Moreover, we show that this peculiar calcium response can be blocked by protein tyrosine kinase inhibitors (herbimycin and genistein) giving evidence of the involvement of a protein tyrosine kinase, the best candidate of which is the CD4-associated p56lck. Altogether, our results suggest that, independently of the TCR/CD3 complex, CD4 may be involved in the triggering of a calcium signal dependent on a protein tyrosine kinase and independent of the phosphoinositide transduction pathway.lld:pubmed
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pubmed-article:9341768pubmed:articleTitleEvidence for a CD4-associated calcium influx independent of the phosphoinositide transduction pathway in human T cells.lld:pubmed
pubmed-article:9341768pubmed:affiliationInstitut National de la Santé et de la Recherche Médicale (INSERM) U431, Université de Montpellier II, France.lld:pubmed
pubmed-article:9341768pubmed:publicationTypeJournal Articlelld:pubmed
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