| The widely studied p53 tumor suppressor gene contains mutations in over 50% of human cancers. p53 protein expression is low in normal cells but increases in response to DNA damage and cellular distress signals. Overexpression of the p53 transcription factor can induce either cell cycle arrest or apoptosis through transcriptional regulation of several genes, including the cell cycle inhibitor p21, DNA repair gene GADD45 and the apoptotic inducer Bax. p53 also induces apoptosis by means of a direct signaling pathway involving the expression of p53AIP1. p53 directly binds to and acts on several cellular proteins involved in various pathways, including c-Abl, basal transcription factor TFIIH and WT1. p53 can be functionally inactivated by mutation, binding to DNA tumor virus encoded proteins, such as SV40 large T antigen, Adenovirus E1B and papilloma virus E6 proteins, or through its interaction with MDM2.This adenovirus express both human p53 and GFP. Reference: Yu J., et al., PNAS (1999) 96: 14517, Chan TA., et al., Genes Dev (00) 14:1584 |
