Tax represses TGF-β1 signaling independently of NF-κB activation or recruitment of CBP/p300.
HepG2 cells were cotransfected with (A) the (CAGA)12-Luc reporter construct (5 μg) and the wild-type Tax (5 μg) or the K88A (5 μg), V89A (5 μg), or M47 (5 μg) mutant expression vectors encoding proteins unable to bind CBP/p300 and p/CAF, respectively. In inset, Tax (5 μg), K88A (5 μg), V89A (5 μg), or M47 (5 μg) constructs were cotransfected with HTLV-I LTR Luc (2 μg) to assess their functional capacities. When indicated, increasing amounts (0.2, 0.5, or 2 μg) of a p300 expression vector alone or in combination with a Tax construct (5 μg) were cotransfected. (B) the (CAGA)12-Luc reporter (2 μg) and wild-type Tax (5 μg), M22 (5 μg), or G148V (5 μg) mutant expression vectors. In inset, Tax (5 μg), M22 (5 μg), or G148V (5 μg) constructs were cotransfected with an NF-κB–responsive reporter gene.
