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. 1998 Nov 10;95(23):13501–13506. doi: 10.1073/pnas.95.23.13501

Figure 3.

Figure 3

The HAT domain of PCAF is required, but not sufficient, to stimulate promoter activity. (A) Deletions within the N or C terminus of PCAF abrogate the ability of PCAF to enhance the Sp1-driven reporter gene. Two deletions within Gal4-PCAF were tested: ΔHAT(574–608), a Gal4-PCAF mutant containing a deletion within the HAT domain of the C-terminal portion of PCAF; and ΔN(65–112), a Gal4-PCAF mutant containing a deletion of amino acids 65–112 within the N-terminal portion of PCAF. RNA from transfected B78 cells was tested with S1-nuclease protection assays. (B) HAT activity in vitro. Wild-type and mutant PCAF proteins were tested for acetyltransferase activity in vitro.