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. 2009 Mar 16;29(10):2644–2657. doi: 10.1128/MCB.00073-09

FIG. 4.

FIG. 4.

TAFH and NHR2 cooperatively target DES to repress transcription in vivo. (A) GST pull-down analyses of in vitro-translated Gal4-HEB-DES (i.e., amino acids 100 to 306) and Gal4-HEB-AD1 with GST, GST-TAFH, or GST-TAFH-K98E. (B) Luciferase assays of 293T cells transfected with ETO, ETO mutants, or their VP16 fusions along with Gal4-DBD or Gal4-HEB(100-306), as well as the Gal4 UAS-driven reporter. WT, wild type. (C) Luciferase assays of 293T cells transfected with ETOΔTAFH (ΔTAFH), ETO-K98E (K98E), or their VP16 fusion proteins, along with Gal4-DBD or Gal4-HEB(100-306) and the Gal4 UAS-driven reporter. (D) Schematic representation showing that the K98E mutation selectively abolishes AD1 interaction. (E and F) Luciferase assays of 293T cells transfected with an E-box-driven reporter and expression vector for HEBΔAD1(E) or E47(F), with ETO and ETO mutants indicated at the bottom.