Cardiac hypertrophy and histone deacetylase–dependent transcriptional repression mediated by the atypical homeodomain protein Hop
J. Clin. Invest. Hyun Kook, et al. 112:863 doi:10.1172/JCI19137 [Go to this article.]

Figure 2
Early lethality and cardiac hypertrophy induced by Hop, but not by mutant HopH2. (a) Kaplan-Meier plot revealing reduced survival of Hop transgenic mice (TgHop wt) compared with wild-type and HopH2 transgenic mice (TgHop H2). (b) Cardiac hypertrophy in Hop transgenic mice is progressive. Heart weight–to–body weight ratios were calculated at various ages, as indicated, and expressed as percentage of change compared with wild-type littermates. Values from two independent transgenic lines are pooled and each bar represents the average of 8–16 data points. Error bars represent SEM. *P < 0.05 compared with wild type. (c) Circular dichroism analysis of Hop and HopH2 protein indicates similar conformations and α helicity of wild-type Hop and HopH2 mutant proteins. (θ)_MRW, mean residue weight ellipticity. (d). Heart weight–to–body weight ratios of Hop transgenic mice, four independent lines of HopH2 transgenic mice, and Hop knockout mice between 4 and 8 weeks of age. Between 10 and 25 animals were assayed for each condition. No significant difference between transgenic and nontransgenic littermates was determined for HopH2 mice or for Hop^–/– mice. Western blot analysis of heart tissue using anti-hemagglutinin (HA) antibody revealing expression of transgenic protein is also shown. Line numbers refer to independent transgenic lines. (e) Immunohistochemistry identifies nuclear epitope-tagged Hop protein in transgenic hearts (red). (f) HopH2 is also nuclear localized in transgenic hearts. Scale bars in e and f: 20 μm.