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. 2013 Apr 24;2(2):e000093. doi: 10.1161/JAHA.113.000093

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© 2013 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley-Blackwell.

This is an Open Access article under the terms of the Creative Commons Attribution Noncommercial License, which permits use, distribution, and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Figure 7. — NTM suppresses Niemann‐Pick C1‐like 1 (NPC1L1) protein expression in the liver, whereas nuclear transport of histone deacetylase 3 (HDAC3) protein is not reduced. Immunoblots of liver extracts from ldlr^−/− mice fed a Western diet and treated with saline control (S) or cSN50.1 peptide (P) by osmotic pump for 8 weeks. Each panel shows samples from the same membrane. A, NPC1L1 in whole‐cell liver extracts. Quantitative analysis of immunoblot indicates significant suppression of NPC1L1 protein in NTM‐treated animals expressed as its relative ratio to β actin loading control. Shown are the mean+SEM of 4 mice/group (*P<0.05 by Mann–Whitney test). B, HDAC3 in liver nuclear extracts. Quantitative analysis of immunoblot indicates no significant difference (by Mann–Whitney test) between HDAC3 protein in saline versus cSN50.1 peptide‐treated mice. HDAC3 protein (green) is expressed as its relative ratio to β actin loading control (red). Shown are the mean+SD of 5 mice/group. NTM indicates nuclear transport modifier; ldlr^−/−, low‐density lipoprotein receptor deficient.