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All rights reserved. http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAXYaNsW040k-CW5CGxW_LQ3p0vP95iXfVjDZUfBamzHw#_6 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RAXYaNsW040k-CW5CGxW_LQ3p0vP95iXfVjDZUfBamzHw#_5 http://www.w3.org/ns/prov#value Dual luciferase assay of PLC/PRF/5 cells transiently transfected with construct I-b1 mutated at the HNF1 site (construct I-b1[HNF1]mut; Figure 5) indicated that abrogation of the HNF1 element results in low promoter activity, with no response to the combination of UDCA and dexamethasone or to either of these compounds alone (Figure 11A). The fact that baseline transcriptional activity of construct I-b1[HNF1]mut was also markedly attenuated compared with that of the wild-type construct (4.5-fold; Figure 11A) suggested that an HNF1-bound transcription factor forms part of the baseline transcription machinery of AE2 {SLC4A2}alternate promoter in intact liver cells. 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