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. Author manuscript; available in PMC: 2014 Nov 1.
Published in final edited form as: Biol Psychiatry. 2013 May 7;74(9):696–705. doi: 10.1016/j.biopsych.2013.03.020

Figure 2.

Figure 2

Adeno-associated virus, serotype 9 capsid-mediated HDAC1 expression and activity. (A, C) Western blots against HDAC1 on (A) prefrontal cortex lysates from (left) control and (right) adeno-associated virus-Hdac1 mice; notice increased 60 kDa immunoreactivity corresponding to full-length HDAC1 but not for lower molecular weight (background) band (B) mouse N1E-115 neuroblastoma cells, showing (top image) increased 60 kDa HDAC1 in transfected (T) compared to control (C) cells. Lower image shows 42 kDa β-actin as loading control. (C) (Top) β-actin loading control and (bottom) bulk histone acetylation in anti-acetyl-lysine K immunoblots from N1E-115 cells, 24 hours posttransfection with Hdac1 (right) and control (left side). Lower band, histone H4ac, and upper band, H3ac. Notice decreased H3 and H4 acetylation in the Hdac1 transfected cells (black), relative to control cells (white bars), as summarized in the bar graph for quantification of acetyl-histones. Optical densities from immunoblots were normalized with β-actin levels and expressed as percentage of the control values. n = 3 per group. *p < .05, **p < .01, paired t test.