Hepatitis B Virus X Protein Induces RNA Polymerase III- Dependent Gene Transcription and Increases Cellular TATA- Binding Protein by Activating the Ras Signaling Pathway

摘要: Our previous studies have shown that the hepatitis B virus protein, X, activates all three classes of RNA polymerase III (pol III)-dependent promoters by increasing cellular level TATA-binding protein (TBP) (H.-D. Wang et al., Mol. Cell. Biol. 15:6720-6728, 1995), a limiting transcription component (A. Trivedi 16:6909-6916, 1996). We investigated whether these X-mediated events are dependent on activation Ras/Raf-1 signaling pathway. Transient expression dominant-negative mutant Ras gene (Ras-ala15) in Drosophila S-2 stable cell line expressing X (X-S2), or incubation cells with farnesylation inhibitor, specifically blocked both X-dependent cotransfected tRNA and increase TBP levels. constitutively activated form (Ras-val12) control S2 produced an These not type specific since induction was also to be rat 1A X. Furthermore, increases pol III-dependent activity levels could restored X-S2 Ras-ala15 coexpressing Raf-1. serum dependent, when deprived, effects augmented. Together, results demonstrate genes cascade. In addition, define two new important consequences mediated signal transduction pathway: central factor, TBP, activity.