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. 2002 Nov;22(22):7929–7941. doi: 10.1128/MCB.22.22.7929-7941.2002

FIG. 1.

FIG. 1.

GILZ overexpression inhibits the binding of AP-1 to its DNA motif. (A) EMSA was performed with nuclear extract from untreated and anti-CD3-treated (1 μg/ml, 1 h) 3DO cells (lanes 2 and 6) or pcDNA3-transfected PV6 (lanes 3 and 7), pcDNA3-GILZ-transfected ST7 (lanes 4 and 8), or GIRL-19 (lanes 5 and 9) clones. Lane 1, probe alone. (B) Nuclear extract from untreated or anti-CD3-treated 3DO cells, alone (lane 5) or added with competitor cold probe (lane 3), with anti-c-Jun (lane 4), or with anti-c-Fos antibody (lane 6). Lane 1, labeled probe alone. C, untreated cells. (C) EMSA performed with NF-AT as the probe. Nuclear extract from untreated and anti-CD3-treated (1 μg/ml, 1 h) 3DO cells (lanes 2 and 6) or PV6 (lanes 3 and 7), ST7 (lanes 4 and 8), or GIRL-19 (lanes 5 and 9) clones. Lane 1, probe alone. The results are representative of three experiments. (D) 3DO cells were transfected with the AP-1 luciferase reporter geneand pcDNA3 (solid bar) or with the reporter gene and pcDNA3-GILZ (open bar) and stimulated for 4 and 18 h with plastic-bound anti-CD3 MAb. The values are expressed as the increase (n-fold) in luciferase activity. Each transfection was performed in triplicate. The standard errors were <10%.