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. Author manuscript; available in PMC: 2006 Jan 25.
Published in final edited form as: Biochem Pharmacol. 2003 Nov 1;66(9):1755–1768. doi: 10.1016/s0006-2952(03)00542-2

FIGURE 5.

FIGURE 5

A. OSI-2040 treatment increases histone H4 acetylation in K562 cells. K562 cells were treated for 24 hours with maximally acting concentration of OSI-97345 (lane 1), OSI-102695 (lane 2), OSI-22121 (lane 3), OSI-101820 (lane 4), OSI-168992 (lane 5), OSI-168996 (lane 6), OSI-168961 (lane 7), OSI-169050 (lane 8), OSI-169170 (lane 9), OSI-2040 (lane 10) or 0.2% DMSO (lane 11). Extracts were subjected to SDS-PAGE, transferred to nitrocellulose and probed with anti-acetyl histone H4 antibody (Upstate Biotechnology, VA). Acetyl-histone H4 (11 kDa) was observed extracts from OSI-2040 treated cells, but not in extracts from cells exposed to 0.2% DMSO or compounds OSI-97345 – OSI-169170. Weak reactivity of the antibody to acetylated-histone H2B (14 kDa) may contribute to band broadening. B. Proprionic hydroxamic acid stimulates histone H4 acetylation in K562 cells. K562 cells were treated for 24 hours with 0.2% DMSO vehicle (lane 1), 10 uM proprionic hydroxamic acid (lane 2), 100 uM proprionic hydroxamic acid (lane 3), 1 uM OSI-2040 (lane 4) histones extracted and probed with anti-Ac histone antibody as described for Figure 5A. The OSI-2040 concentration of 1 uM provides maximal γ-globin inducing activity yet was below the 24 hour cytotoxic IC50.