Publication | Open Access
Synergism between distinct enhanson domains in viral induction of the human beta interferon gene.
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Citations
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References
1990
Year
Irf-1 Transcription FactorGeneticsViral ImmunityViral PathogenesisImmunologyPromoter TemplateProtein ExpressionVirus GeneViral InductionViral GeneticsVirologyHuman Beta InterferonGene ExpressionCell BiologyPathogenesisAntiviral ResponseVirus-host InteractionSystems BiologyMedicineDistinct Enhanson Domains
This study demonstrates distinct virus-inducible enhanson properties for three regions of the human beta interferon (IFN-beta) promoter; maximum virus inducibility required syngerism among all three enhansons. Expression of the IRF-1 transcription factor differentially increased the expression of plasmids containing (AAGTGA)4 or PRDIII (-94 to -78) motifs but was inefficient in the induction of the intact IFN-beta promoter. The human T-cell lymphotropic virus type I Tax protein was a strong positive activator of PRDII (-64 to -55)-containing plasmids but was also unable to stimulate the IFN-beta promoter. Induction of the intact IFN-beta promoter linked to a reporter plasmid was achieved in lymphoid and epithelioid cellular backgrounds by a triple transfection with IRF-1 and Tax expression plasmids or a combination of IRF-1 and phorbol ester, indicating that at least two trans-activating events and the association of two proteins on the promoter template are required for IFN-beta activation.
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