Abstract
v-Src activates promoters under the control of 12-O-tetradecanoylphorbol-13-acetate (TPA) response elements (TREs) and serum response elements (SREs) via two distinguishable intracellular signaling mechanisms. The induction of TRE- and SRE-mediated gene expression by v-Src could be distinguished by a differential sensitivity to depleting cells of protein kinase C (PKC) and to a dominant negative Raf-1 mutant. Thus, PKC depletion and the dominant negative Raf-1 mutant were able to distinguish two intracellular signaling mechanisms activated by v-Src. Both of these v-Src-induced intracellular signals were sensitive to a dominant negative mutant of Ha-Ras. These data suggest that Ha-Ras functions to coordinately regulate multiple intracellular signaling mechanisms activated by v-Src.
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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3T3 Cells
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Animals
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Chloramphenicol O-Acetyltransferase / genetics
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Chloramphenicol O-Acetyltransferase / metabolism
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Cloning, Molecular
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GTPase-Activating Proteins
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Gene Expression Regulation*
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Genes, ras*
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Genes, src*
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Mice
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Plasmids
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Promoter Regions, Genetic* / drug effects
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Proteins / metabolism
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Recombinant Proteins / metabolism
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Restriction Mapping
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Simplexvirus / enzymology
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Simplexvirus / genetics
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Tetradecanoylphorbol Acetate / pharmacology
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Thymidine Kinase / genetics
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Transcription, Genetic
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Transfection
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ras GTPase-Activating Proteins
Substances
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GTPase-Activating Proteins
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Proteins
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Recombinant Proteins
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ras GTPase-Activating Proteins
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Chloramphenicol O-Acetyltransferase
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Thymidine Kinase
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Tetradecanoylphorbol Acetate