ETS1, NFκB and AP1 synergistically transactivate the human GM–CSF promoter
RS Thomas, MJ Tymms, LH McKinlay, MF Shannon… - Oncogene, 1997 - nature.com
RS Thomas, MJ Tymms, LH McKinlay, MF Shannon, A Seth, I Kola
Oncogene, 1997•nature.comActivation of helper T cells results in coordinate expression of a number of cytokines
involved in differentiation, proliferation and activation of the haematopoietic system.
Granulocyte-macrophage colony stimulating factor (GM–CSF) is one such cytokine, whose
increased expression results mostly from increases in transcription. Cis-acting elements with
NFκB, AP1 and ETS-like binding motifs have been identified in the promoter region of the
GM–CSF gene, and are important or essential for transcriptional activity following T cell …
involved in differentiation, proliferation and activation of the haematopoietic system.
Granulocyte-macrophage colony stimulating factor (GM–CSF) is one such cytokine, whose
increased expression results mostly from increases in transcription. Cis-acting elements with
NFκB, AP1 and ETS-like binding motifs have been identified in the promoter region of the
GM–CSF gene, and are important or essential for transcriptional activity following T cell …
Abstract
Activation of helper T cells results in coordinate expression of a number of cytokines involved in differentiation, proliferation and activation of the haematopoietic system. Granulocyte-macrophage colony stimulating factor (GM–CSF) is one such cytokine, whose increased expression results mostly from increases in transcription. Cis-acting elements with NFκB, AP1 and ETS-like binding motifs have been identified in the promoter region of the GM–CSF gene, and are important or essential for transcriptional activity following T cell activation. ETS1 is a transcription factor of the ETS family that is expressed in T cells. We have previously shown that ETS1 can transactivate GM–CSF in Jurkat T cells, but only after the cells have been stimulated by treatment with PMA and ionomycin, agents that mimic T cell activation. Thus we proposed that ETS1, which is expressed constitutively in Jurkat cells, may act in concert with PMA/ionomycin inducible factors. Here we show that ETS1 can transactivate a GM–CSF reporter construct in unstimulated Jurkat cells, providing that either NFκB or AP1 transcription factors are supplied by co-transfection. We confirm that binding of endogenous NFκB and AP1 is induced following PMA/ionomycin treatment of T cells. Transactivation by ETS1, NFκB and AP1 is synergistic, and mutation of the individual binding sites reveals that the transcriptional activities of these factors are inter-dependent. Our results suggest that constitutive ETS1, and inducible NFκB and AP1, cooperate as part of a higher order transcriptional complex in activated T cells.
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