In:
European Journal of Biochemistry, Wiley, Vol. 246, No. 1 ( 1997-05), p. 142-146
Abstract:
To determine the regulatory mechanism of the expression of the mouse platelet‐derived growth factor (PDGF) β‐receptor gene, a 1.9‐kb 5′ flanking genomic fragment was cloned and analyzed. Site‐directed mutagenesis of a CCAAT motif, located 60 bp upstream of the transcriptional‐start site, completely abolished the promoter activity [ Ballagi, A. E., Ishisaki, A., Nelin, J.‐O. & Funa, K. (1995) Biochem. Biophys. Res. Commun. 210 , 165–175]. The sequence around the intact CCAAT motif was protected by in vitro DNase‐I‐footprinting analysis. Electrophoresis‐mobility‐shift assays with anti‐[nuclear factor Y(NF‐Y)]Ig revealed binding of the NF‐Y complex to the CCAAT box. Furthermore, the double‐stranded oligonucleotides corresponding to the sequence around the CCAAT motif were conjugated with DNA‐affinity magnetic beads. The binding proteins were affinity purified and identified as the NF‐Y transcription factor by western blotting. Our results indicate that NF‐Y controls the basal transcription activity of the mouse PDGF β‐receptor gene.
Type of Medium:
Online Resource
ISSN:
0014-2956
,
1432-1033
DOI:
10.1111/ejb.1997.246.issue-1
DOI:
10.1111/j.1432-1033.1997.t01-2-00142.x
Language:
English
Publisher:
Wiley
Publication Date:
1997
detail.hit.zdb_id:
1398347-7
detail.hit.zdb_id:
2172518-4
SSG:
12
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