作者: Yu-ling Wu , John W Mehew , Caroline A Heckman , Magdalena Arcinas , Linda M Boxer
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摘要: The p53 protein activates promoters containing binding sites, and it represses other promoters. We examined the effect of on bcl-2 expression in both DHL-4 B cell line K562 erythroleukemia line. Transient transfection analyses revealed that wild-type repressed full-length promoter. region promoter was responsive to mapped P2 minimal region, we showed TATA bound sequence. protein, p53, histone deacetylase-1 mSin3a could be co-immunoprecipitated from nuclear extract. recovered a complex at sequence, however, formation this not dependent presence p53. Treatment cells with deacetylase inhibitor, trichostatin A, resulted an increase activity whether present or not. Therefore, demonstrated deacetylases repress independently. Similar results were obtained when endogenous mRNA levels measured response either enhanced apoptosis. RNase protection assays transcription 3' decreased by regions required for repression defined. conclude sequence is target interaction between TBP most likely responsible repression. Mutation may play role up-regulation some lymphomas.