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. Author manuscript; available in PMC: 2009 Nov 16.
Published in final edited form as: Science. 2009 Apr 17;324(5925):407–410. doi: 10.1126/science.1164265

Fig. 1.

Fig. 1

GBSs differentially direct GR activity. (A) GBSs were cloned upstream of a minimal SV40 promoter driving luciferase. Transcriptional activities and binding affinities (humanGR-DBD 380 to 540) for each GBSs ± SEM are shown [number of independent experiments (n) ≥ 3]. KD, dissociation constant. (B) GBS- specific patterns of domain utilization. GBS reporters respond differentially to mutations in Dim (red, A477T), AF1 (yellow, E219K/F220L/W234R), and AF2 (green, E773R) domains. Fold induction by dex ± SEM (top) and percent induction by mutant GR relative to wild type (bottom) are shown (n ≥ 3). (C) Immunoblots demonstrating short hairpin–mediated RNA (shRNA) knock-down of Brm and CARM1. (D) GBS inductions after CARM1 or Brm knock-down, relative to scrambled shRNA ± SEM, are shown (n = 3).