Title : No point mutation of Ha-ras or p53 genes expressed in preneoplastic-to-neoplastic progression as modeled in mouse JB6 cell variants.

Pub. Date : 1993

PMID : 8352891






4 Functional Relationships(s)
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1 Both p53-hybridizing transcripts were downregulated by prolonged 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment (24 h) regardless of the stage of progression. Tetradecanoylphorbol Acetate tumor protein p53 Homo sapiens
2 Both p53-hybridizing transcripts were downregulated by prolonged 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment (24 h) regardless of the stage of progression. Tetradecanoylphorbol Acetate tumor protein p53 Homo sapiens
3 We conclude from this study that in JB6 variants (1) mutational activation of Ha-ras and inactivation of p53 are unlikely to be involved in preneoplastic progression; (2) increased amounts of p53 protein may be involved in a subset of transformed cells, possibly reflecting a longer half-life, as demonstrated in other systems; and (3) late downregulation of p53 mRNA but not protein expression may be a secondary response in the TPA-mediated signal transduction pathway. Tetradecanoylphorbol Acetate tumor protein p53 Homo sapiens
4 We conclude from this study that in JB6 variants (1) mutational activation of Ha-ras and inactivation of p53 are unlikely to be involved in preneoplastic progression; (2) increased amounts of p53 protein may be involved in a subset of transformed cells, possibly reflecting a longer half-life, as demonstrated in other systems; and (3) late downregulation of p53 mRNA but not protein expression may be a secondary response in the TPA-mediated signal transduction pathway. Tetradecanoylphorbol Acetate tumor protein p53 Homo sapiens