Abstract
LMP2A is expressed in latent Epstein-Barr virus (EBV) infection and interacts with LMP1 and members of the src tyrosine kinase family in the plasma membrane. Since tyrosine kinase mediate receptor-induced changes in intracellular free calcium, the effect of LMP2A on receptor-mediated intracellular calcium mobilization was evaluated by stably expressing LMP2A in an EBV-negative Burkitt tumor cell line (BJAB) or in LMP1-converted BJAB cells. LMP2A significantly blocked calcium mobilization following class II, CD19, or immunoglobulin M cross-linking. LMP2A effects were partially reversed in LMP1-converted cell lines. These results are compatible with LMP2A acting in latent B-lymphocyte infection to downmodulate LMP1 effects on cell growth or to inhibit induction of lytic EBV infection in specific human tissues following receptor ligation.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Antigens, CD / metabolism
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Antigens, CD19
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Antigens, Differentiation, B-Lymphocyte / metabolism
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Antigens, Viral / genetics
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Antigens, Viral / metabolism*
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Antigens, Viral / pharmacology
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B-Lymphocytes / drug effects
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B-Lymphocytes / metabolism*
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Burkitt Lymphoma
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Calcium / metabolism*
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Down-Regulation
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Flow Cytometry
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Genes, MHC Class II
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Humans
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Immunoglobulin M / metabolism
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Lymphocyte Activation / physiology*
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Receptors, Cell Surface / metabolism
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Transfection
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Tumor Cells, Cultured
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Viral Matrix Proteins / genetics
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Viral Matrix Proteins / metabolism*
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Viral Matrix Proteins / pharmacology
Substances
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Antigens, CD
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Antigens, CD19
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Antigens, Differentiation, B-Lymphocyte
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Antigens, Viral
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EBV-associated membrane antigen, Epstein-Barr virus
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Immunoglobulin M
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Receptors, Cell Surface
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Viral Matrix Proteins
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Calcium