Overexpression of cardiac actin with baculovirus is promoter dependent.
The influence of the promoter and an N-terminal hexahistidine tag on human cardiac actin (ACTC) expression and function was investigated using four baculovirus constructs. It was found that both non-tagged ACTC and hisACTC expression from the p10 promoter was higher than from the polh promoter. Characterization showed that an N-terminal hexahistidine tag has a negative effect on ACTC. Recombinant ACTC inhibits DNase-I and binds myosin S1, indicative of proper folding. Our data support the hypothesis that the actin protein down-regulates the polh promoter.