HATs off to Hop: recruitment of a class I histone deacetylase incriminates a novel transcriptional pathway that opposes cardiac hypertrophy
J. Clin. Invest. Yasuo Hamamori, et al. 112:824 doi:10.1172/JCI19834 [Go to this article.]

Figure 1
Complementary functions of class I and class II HDACs in cardiac hypertrophy. (a) The myocyte enhancer factor-2–based transcriptional program that triggers cardiac hypertrophy is repressed by signal-responsive class II HDACs, which are exported from the nucleus as the result of hypertrophic cues (1, 2). (b) A class I HDAC (HDAC2) is recruited to SRF — via Hop as an intermediary — thereby blocking a transcriptional program that opposes hypertrophy (14). MEF2, myocyte enhancer factor-2.