Synergy between the NF-E1 erythroid-specific transcription factor and the CACCC factor in the erythroid-specific promoter of the human porphobilinogen deaminase gene.
A 114-base-pair promoter fragment of the human porphobilinogen deaminase gene functioned in an erythroid-specific manner in transient transfection experiments. Site-directed mutagenesis of the binding site for the erythroid-specific transcription factor (NF-E1) or an adjacent CACCC motif abolished the promoter activity. Increasing the spacing between these sites progressively reduced promoter activity, but there was no evidence that a critical alignment of the two factors on the DNA helix was required.
Frampton
J
J
Cancer Research Campaign Beatson Laboratories, Beatson Institute for Cancer Research, Bearsden, Glasgow, Scotland.
Walker
M
M
Plumb
M
M
Harrison
P R
PR
D000642:Ammonia-Lyases / Q000235:genetics*; D001483:Base Sequence; D001665:Binding Sites; D002872:Chromosome Deletion; D004268:DNA-Binding Proteins / Q000378:metabolism*; D050981:Erythroid-Specific DNA-Binding Factors; D005786:Gene Expression Regulation; D005796:Genes; D005822:Genetic Vectors; D006801:Humans; D011163:Hydroxymethylbilane Synthase / Q000235:genetics*; D008969:Molecular Sequence Data; D009154:Mutation; D015345:Oligonucleotide Probes; D011401:Promoter Regions, Genetic; D014157:Transcription Factors; D014162:Transfection
D004268:DNA-Binding Proteins; D050981:Erythroid-Specific DNA-Binding Factors; D015345:Oligonucleotide Probes; D014157:Transcription Factors; D011163:Hydroxymethylbilane Synthase; D000642:Ammonia-Lyases