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. 2010 Jun 1;101(9):2019–2025. doi: 10.1111/j.1349-7006.2010.01636.x

Figure 1.

Figure 1

 Hakai functions as a corepressor of estrogen receptor (ER)‐α. (a) GAL4N‐Hakai fusion protein functions as a transcriptional repressor, which is independent from the recruitment of histone deacetylase (HDAC) activity. Cos‐7 cells were cotransfected with GAL4N or GAL4N‐fused Hakai with the reporter Gal4‐tk‐luc. Cells were treated with or without 100 nM trichostatin A (TSA), an inhibitor of HDAC. (b) Hakai significantly represses the transactivation of ERα in Cos‐7 cells transiently transfected with the expression construct of nuclear receptors together with a corresponding reporter. (c) E3 ubiquitin‐ligase activity of Hakai is not required for the inhibition of ERα transactivation in transiently transfeced Mcf‐7 cells. Schematic diagram of Hakai with domains is shown. (d) Hakai inhibits the expression of an ERα target gene, pS2, in Mcf‐7/Hakai stable cell line, in which Hakai expression is induced by the treatment of doxycycline (300 ng/mL). (e) The expression of Hakai shRNA relieved the Hakai‐mediated inhibition of ERα transactivation in Mcf‐7/Hakai cells. Filled boxes indicate the presence of 100 nM estradiol, testosterone, or 9‐cis retinoic acid. *P < 0.05 and **P < 0.005, significant differences from the control.