Suppression of senescence in normal human fibroblasts by introduction of dominant-negative p53 mutants or human papilloma virus type 16 E6 protein.
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.
Division of Biochemistry, Kihara Institute for Biological Research, Yokohama, Japan.
A
A
Ide
M
M
Fujii
K
K
Nakababashi
D
D
Ayusawa
D016922:Cellular Senescence / Q000187:drug effects* / Q000235:genetics; D003114:Colony-Forming Units Assay; D005347:Fibroblasts / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D009856:Oncogene Proteins, Viral / Q000235:genetics / Q000494:pharmacology*; D027383:Papillomaviridae; D010957:Plasmids; D012097:Repressor Proteins; D014162:Transfection; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000494:pharmacology*
C068651:E6 protein, Human papillomavirus type 16; D009856:Oncogene Proteins, Viral; D012097:Repressor Proteins; D016159:Tumor Suppressor Protein p53