UV irradiation increases p53 levels in nontransformed mouse cells. Warren Maltzman and Linda Czyzik investigated how UV light and a UV-mimetic chemical carcinogen, 4-nitroquinoline-1-oxide (4NQO), affect p53 levels in nontransformed and transformed mouse cells. They found that both treatments caused a rapid increase in p53 levels, which they attributed to post-translational stabilization of p53, independent of replicative DNA synthesis. This suggests that p53 is not an accidental product of proliferating cells but is involved in preparing mammalian cells for DNA synthesis. p53 is a cellular protein first observed in SV40-transformed mouse cells. It is elevated in various systems, including cells transformed by DNA tumor viruses, isolated from naturally occurring tumors, or stimulated by mitogens or serum factors to synthesize DNA. The correlation between high p53 levels and transformation events or other treatments that stimulate cellular growth supports the hypothesis that p53 functions in the regulation of the transition of mammalian cells to active proliferation. However, the molecular mechanism by which p53 affects this transition is not yet known. In SV40-transformed mouse cells, elevated p53 levels are due to the tight interaction between p53 and the SV40-encoded large tumor antigen (T-Ag), which increases the half-lives of both proteins. This interaction suggests that p53 functions in the regulation of cellular growth by interacting with viral transforming gene products in virus-transformed cells and with a cellular protein in normal cells. The regulation of p53 expression in neoplasticly transformed cells has been most extensively examined in SV40-transformed mouse cells. The elevated levels of p53 in these cells are due to the interaction between p53 and T-Ag, which increases the half-lives of both proteins. This interaction suggests that p53 functions in the regulation of cellular growth by interacting with viral transforming gene products in virus-transformed cells and with a cellular protein in normal cells. The regulation of p53 expression in neoplasticly transformed cells has been most extensively examined in SV40-transformed mouse cells. The elevated levels of p53 in these cells are due to the interaction between p53 and T-Ag, which increases the half-lives of both proteins. This interaction suggests that p53 functions in the regulation of cellular growth by interacting with viral transforming gene products in virus-transformed cells and with a cellular protein in normal cells. The results of the study suggest that p53 may be involved in the initiation of DNA replication. This is supported by several lines of evidence: (i) the viral proteins with which p53 interacts in DNA tumor virus-transformed cells are also required for viral DNA replication; (ii) the stimuli which increase the levels of p53 in nontransformed cells also induce DNAUV irradiation increases p53 levels in nontransformed mouse cells. Warren Maltzman and Linda Czyzik investigated how UV light and a UV-mimetic chemical carcinogen, 4-nitroquinoline-1-oxide (4NQO), affect p53 levels in nontransformed and transformed mouse cells. They found that both treatments caused a rapid increase in p53 levels, which they attributed to post-translational stabilization of p53, independent of replicative DNA synthesis. This suggests that p53 is not an accidental product of proliferating cells but is involved in preparing mammalian cells for DNA synthesis. p53 is a cellular protein first observed in SV40-transformed mouse cells. It is elevated in various systems, including cells transformed by DNA tumor viruses, isolated from naturally occurring tumors, or stimulated by mitogens or serum factors to synthesize DNA. The correlation between high p53 levels and transformation events or other treatments that stimulate cellular growth supports the hypothesis that p53 functions in the regulation of the transition of mammalian cells to active proliferation. However, the molecular mechanism by which p53 affects this transition is not yet known. In SV40-transformed mouse cells, elevated p53 levels are due to the tight interaction between p53 and the SV40-encoded large tumor antigen (T-Ag), which increases the half-lives of both proteins. This interaction suggests that p53 functions in the regulation of cellular growth by interacting with viral transforming gene products in virus-transformed cells and with a cellular protein in normal cells. The regulation of p53 expression in neoplasticly transformed cells has been most extensively examined in SV40-transformed mouse cells. The elevated levels of p53 in these cells are due to the interaction between p53 and T-Ag, which increases the half-lives of both proteins. This interaction suggests that p53 functions in the regulation of cellular growth by interacting with viral transforming gene products in virus-transformed cells and with a cellular protein in normal cells. The regulation of p53 expression in neoplasticly transformed cells has been most extensively examined in SV40-transformed mouse cells. The elevated levels of p53 in these cells are due to the interaction between p53 and T-Ag, which increases the half-lives of both proteins. This interaction suggests that p53 functions in the regulation of cellular growth by interacting with viral transforming gene products in virus-transformed cells and with a cellular protein in normal cells. The results of the study suggest that p53 may be involved in the initiation of DNA replication. This is supported by several lines of evidence: (i) the viral proteins with which p53 interacts in DNA tumor virus-transformed cells are also required for viral DNA replication; (ii) the stimuli which increase the levels of p53 in nontransformed cells also induce DNA