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Related Experiment Videos

Transformation by polyoma virus middle T antigen.

S A Courtneidge

    Cancer Surveys
    |January 1, 1986
    PubMed
    Summary

    Polyoma virus middle T antigen activates cellular tyrosine kinase pp60c-src, but this activation alone doesn't cause transformation. Other middle T interactions are crucial for polyoma virus-induced cell changes.

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    Area of Science:

    • Virology
    • Molecular Biology
    • Cellular Biology

    Background:

    • Polyoma virus middle T antigen is a key viral oncoprotein.
    • Middle T antigen is a membrane-associated phosphoprotein involved in cell transformation.
    • Middle T antigen interacts with cellular tyrosine kinase pp60c-src.

    Purpose of the Study:

    • To investigate the role of middle T antigen-pp60c-src complex formation in polyoma virus transformation.
    • To identify other essential interactions of middle T antigen for cellular transformation.
    • To elucidate the mechanism by which middle T antigen activates pp60c-src.

    Main Methods:

    • Mutant analysis of middle T antigen.
    • Biochemical assays to study protein complex formation and phosphorylation.
    • Enzyme activity measurements of pp60c-src.

    Main Results:

    • Middle T antigen forms a complex with and is phosphorylated by pp60c-src.
    • Middle T binding induces pp60c-src autophosphorylation and increases its specific activity.
    • A non-transforming middle T mutant (dl1015) activates pp60c-src, indicating other factors are necessary for transformation.
    • Middle T may transform cells by associating with phosphatidylinositol kinase and/or a 61 kDa protein.
    • Middle T might interfere with pp60c-src regulation by altering its phosphorylation state.

    Conclusions:

    • Middle T antigen-induced pp60c-src activation is necessary but not sufficient for polyoma virus transformation.
    • Additional interactions of middle T antigen, possibly with phosphatidylinositol kinase or a 61 kDa protein, are critical for oncogenic transformation.
    • Polyoma virus-transformed cells serve as a model for studying pp60c-src regulation and identifying its substrates.

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