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pubmed-article:12385028pubmed:abstractTextThe current model suggesting that raft integrity is required for T cell activation is mostly (but not exclusively) based on the use of drugs, such as methyl-beta-cyclodextrin (M beta CD), that disorganize rafts and inhibit T cell receptor (TCR)-induced Ca2+ influx. Here we show that conditions that disrupt lipid raft integrity do not inhibit TCR triggering in Jurkat cells and normal T lymphocytes. Indeed, we found that the reported inhibition of TCR-induced Ca2+ influx by M beta CD treatment is mainly due to (a) nonspecific depletion of intracellular Ca2+ stores and (b) plasma membrane depolarization of T cells. When these side-effects are taken into account, raft disorganization does not alter TCR-dependent Ca2+ signaling. In line with these results, also TCR-induced tyrosine phosphorylation is not inhibited by dispersion of lipid rafts. By contrast, in the same conditions, Ca2+ signaling via the glycosylphosphatidylinositol (GPI)-anchored protein CD59 is totally abolished. These results indicate that, while signaling through GPI-anchored proteins requires lipid raft integrity, CD3-dependent TCR activation occurs independently of cholesterol extraction.lld:pubmed
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pubmed-article:12385028pubmed:pagination3082-91lld:pubmed
pubmed-article:12385028pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:12385028pubmed:articleTitleLipid rafts and T cell receptor signaling: a critical re-evaluation.lld:pubmed
pubmed-article:12385028pubmed:affiliationDepartment of Biomedical Sciences, University of Padova, Padova, Italy.lld:pubmed
pubmed-article:12385028pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:12385028pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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