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• W1838401124 endingPage "1566" @default.
• W1838401124 startingPage "1561" @default.
• W1838401124 abstract "B cell Ag receptor (BCR) cross-linking with anti-Ig Abs efficiently induces activation of latently infected EBV in some B cell lines, but not in others. The present study was aimed at defining the molecular mechanisms that determine the response to BCR-mediated EBV activation. Comparison of Burkitt's lymphoma-derived Akata, Mutu-I, and Daudi cells, which are representative responders and nonresponders to BCR-mediated EBV activation, respectively, indicated that three signaling pathways, phosphatidylinositol 3-kinase (PI3K), extracellular signal-regulated kinase (ERK), and p38 mitogen-activated protein kinase (MAPK), were activated in anti-Ig-treated Akata and Mutu-I cells. However, in anti-Ig-treated Daudi cells PI3K was not activated, ERK was faintly activated, and p38 MAPK was constitutively phosphorylated irrespective of anti-Ig treatment. Restoration of PI3K activity with insulin-like growth factor 1 restored ERK and p38 MAPK pathways, and was accompanied by EBV activation in anti-Ig-treated Daudi cells. In contrast, a specific inhibitor for PI3K, wortmannin, inhibited EBV activation by anti-Ig Abs in Akata and Mutu-I cells. Transfection assays in EBV-negative Daudi cells revealed that PI3K activated a promoter for BZLF1, which is a switch of EBV activation from a latent infection, in the absence of other EBV products suggesting that the BZLF promoter was a target of BCR signaling, and that PI3K was important for BCR-mediated BZLF1 activation. These results indicate that the absence of PI3K impedes the progression of signals through the BCR and becomes a determinant of unresponsiveness to BCR-mediated EBV activation." @default.
• W1838401124 created "2016-06-24" @default.
• W1838401124 creator A5048138293 @default.
• W1838401124 creator A5068346020 @default.
• W1838401124 date "2004-02-01" @default.
• W1838401124 modified "2023-10-10" @default.
• W1838401124 title "Phosphatidylinositol 3-Kinase Is a Determinant of Responsiveness to B Cell Antigen Receptor-Mediated Epstein-Barr Virus Activation" @default.
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• W1838401124 doi "https://doi.org/10.4049/jimmunol.172.3.1561" @default.
• W1838401124 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/14734735" @default.
• W1838401124 hasPublicationYear "2004" @default.
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