Suppression of senescence in normal human fibroblasts by introduction of dominant-negative p53 mutants or human papilloma virus type 16 E6 protein.

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Transfection of nearly senesced human fibroblasts with plasmids encoding HPV16 E6 protein or dominant-negative p53 mutants greatly increased their colony-forming ability. Isolated colonies with these plasmids showed extension of lifespan compared to those with a control plasmid. These data demonstrate that p53 plays a major role in senescence in normal human fibroblasts.