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. Author manuscript; available in PMC: 2019 Jan 21.
Published in final edited form as: Mol Immunol. 2010 May 11;47(11-12):2094–2102. doi: 10.1016/j.molimm.2010.04.002

Table 1. Transactivation of ECR1_525 by different transcription factors.

Transcription factor A. Fold activation of luciferase reporter in HEK 293 cells B. Percentage of d2EGFP expressing Jurkat T cells
Unstimulated PMA/iono
/   1.1 ± 0.2 1.1   2
AML1a      1 ± 0.2 1   2.7
AML1b   2.8 ± 0.3 1.2   1.9
EAPP   1.7 ± 0.1 1   2.5
E2F1   0.3 ± 0.1 1.4   1.8
E2F4   2.5 ± 0.4 0.9   2.2
EGR1   2.1 ± 0.5 1.4   2.7
Elk1   4.3 ± 0.1 0.7   1.5
Foxp3   1.6 ± 0.2 0.6   2
GATA1   4.7 ± 0.4 1.4   4.5
NFATc1a      1 ± 0.2 1.8   5.1
NFATc2/p   1.4 ± 0.4 1.2   3.1
PU.1   2.7 ± 0.3 2.5   3
p65 24.4 ± 3.9 3.5 10.9
cRel   1.6 ± 0.1 1.3   2.1
STAT1   0.6 ± 0.1 1.5   2.1
STAT5a   1.2 ± 0.4 2.3   4.1
SP1   1.3 ± 0 1,8   2.3
SP3   1.4 ± 0.4 3   1.5

(A) HEK 293 cells were transiently co-transfected with 1 µg ECR1_525 luciferase reporter plasmid alone or in combination with 2 µg of expression vectors encoding the indicated transcription factors. Luciferase expression was measured after 24 h. The data are the mean value ± SD of three independent experiments. (B) Jurkat T cells were electroporated using 2 µg ECR1_525 d2EGFP reporter plasmid in combination with 1 µg of either one of the indicated transcription factor cDNA or as control empty pCIneoHA vector. Samples were divided and treated for 22 h with or without PMA/ionomycin. Prior to flow cytometry measurement, the cells were treated with 1 µg/ml 7-AAD to distinguish dead cells from the living population.