1 un heterodimers were found to optimally bind tetradecanoylphorbol acetate response element (TRE) and

2 ollowing exposure to the tumor promoter 12-O-tetradecanoylphorbol acetate than in P+ cells.

3  to higher levels by the tumor promoter 12-O-tetradecanoylphorbol acetate (TPA) and were sustained lo

4 tandard growth conditions, are unaffected by tetradecanoylphorbol acetate (TPA) induction, and presum

5  that activation of PKC by the phorbol ester tetradecanoylphorbol acetate (TPA) inhibits cell death v

6 tion therapy (XRT) by pretreatment with 12-O-tetradecanoylphorbol acetate (TPA), a known apoptogenic

7 f cells with HNE dose-dependently suppresses tetradecanoylphorbol acetate (TPA)/ionomycin (IM)-induce

8 reated and phorbol 12-myristate 13-acetate ('tetradecanoylphorbol acetate', TPA) treated K562 cells,

9                             However, in TPA (tetradecanoylphorbol acetate)-treated cells, TLK16998 bu