Abstract
Immature T cells and some T cell hybridomas undergo apoptotic cell death when activated through the T cell receptor complex, a phenomenon that is probably related to antigen induced negative selection of developing T cells. This activation-induced apoptosis depends on active protein and RNA synthesis in the dying cells, although none of the genes required for this process have previously been identified. Antisense oligonucleotides corresponding to c-myc block the constitutive expression of c-Myc protein in T cell hybridomas and interfere with all aspects of activation-induced apoptosis without affecting lymphokine production in these cells. These data indicate that c-myc expression is a necessary component of activation-induced apoptosis.
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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Animals
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Antigens, Differentiation, T-Lymphocyte / physiology
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Base Sequence
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Blotting, Western
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CD3 Complex
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Cell Death / drug effects
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Cell Death / genetics
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Flow Cytometry
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Gene Expression / drug effects
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Genes, fos / physiology
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Genes, myc / physiology*
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Hybridomas
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Lymphocyte Activation / drug effects
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Lymphocyte Activation / physiology*
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Molecular Sequence Data
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Oligonucleotides, Antisense / genetics
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Oligonucleotides, Antisense / pharmacology
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Proto-Oncogene Proteins c-myc / biosynthesis
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RNA / biosynthesis
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Receptors, Antigen, T-Cell / physiology
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T-Lymphocytes / physiology*
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Transcription, Genetic
Substances
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Antigens, Differentiation, T-Lymphocyte
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CD3 Complex
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Oligonucleotides, Antisense
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Proto-Oncogene Proteins c-myc
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Receptors, Antigen, T-Cell
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RNA