We also study the role of STAT1 in untreated cells, where it is required for efficient constitutive expression of many genes, including caspases 1-3 and LMP2. Unphosphorylated STAT1 forms dimers with itself and other transcription factors, activating the expression of promoters with complex DNA elements. Using p53-responsive promoters, we have isolated several mutant cells in which p53 signaling is altered. Although the lesion in AP14 is not yet known, its phenotype clearly establishes a link between growth factor-activated MAP kinase signaling and the capacity of cells to utilize the regulatory functions of p53. Biochemical and cell cycle analyses have helped to reveal the complexity of p53 action.
Different stimuli lead to different patterns of phosphorylation.
USA 95, 14775-14780. Mechanisms of G2 arrest in response to overexpression of p53. Functional approaches to gene discovery.