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We have previously described ECIF-1, a DNA-binding factor present in nuclear extracts of murine embryonal carcinoma cells which specifically recognizes a region within the human beta-interferon promoter. We show that the promoter region located between -112 and -93 is sufficient for this binding activity, which is not due to binding of interferon-regulatory factor 1 or 2. By mutational analysis of the ECIF-1 site, it was determined that the central nucleotides which are critical for binding contain an octameric motif: ATTTACAT. The binding activity of ECIF-1 with its cognate site within the beta-interferon promoter decreases upon differentiation concurrently with the onset of interferon inducibility. Furthermore, by using an in vitro transcription assay with deleted promoter elements of the beta-interferon gene, we show that undifferentiated P19 nuclear extracts contain a repressing activity which depends on the presence of the ECIF-1 site. This repression is not observed using nuclear extracts from differentiated P19 cells. Comparison of the binding activity of this octamer site with others previously shown to be active in embryonal carcinoma cells reveals similarities and differences in the spectrum of proteins binding there.
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R Camato, and
G Paterno, and
L Cohen, and
J Hiscott, and
D Skup
January 1991,
Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer,
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November 1990,
Differentiation; research in biological diversity,
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August 1989,
Molecular and cellular biology,
A Haggarty, and
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Nucleic acids research,
A Haggarty, and
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September 1990,
Development (Cambridge, England),
A Haggarty, and
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June 1993,
Oncogene,
A Haggarty, and
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January 1994,
Developmental genetics,
A Haggarty, and
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J Hiscott, and
D Skup
August 1985,
Cell differentiation,
A Haggarty, and
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D Skup
September 1999,
Molecular and cellular biochemistry,
