The atrial natriuretic peptide receptor ( @entity28353 ) Is expressed in smooth muscle cells of the vasculature, where it is thought to signal the vasodilatory properties of the peptide. Despite its important role as a regulator of cardiovascular homeostasis, relatively little is known of the genomic factors governing expression of this gene. We show here that @entity28353 promoter activity is reduced by 50-75% when any of three GC-rich sites are mutated. Simultaneous mutation of all three leads to a >90% reduction in @entity28353 promoter activity. Transfection of wild-type, but not mutant, decoy oliogonucleotides encoding any one of the sites reduces @entity28353 activity, presumably reflecting competition for a common transcription factor. Gel shift analyses show that each of the wild-type, but not the mutant, sites interferes with the formation of selected DNA-protein complexes on the other sites. These complexes share similar electrophoretic mobility. Immunoperturbation studies show that one of these shared complexes contains @entity10564 , whereas two others contain @entity41023 . Overexpression of either @entity10564 or @entity41023 in a cell type containing very low levels of these transcription factors (i.e. @entity238 Schneider cells) leads to induction of the wild-type, but not the mutant, @entity28353 promoter. The data suggest that the @entity10564 family of transcription factors plays a central role in @entity28353 gene transcription. The association of @entity10564 family members with transcriptional regulation of a number of genes involved in hemodynamic control will be discussed.

XXXX dependence of natriuretic peptide receptor A gene transcription in rat aortic smooth muscle cells.

@entity28353 :: ('24603(Tax:10116)', 'Gene') :: ['NPR-A'] @entity41023 :: ('367846(Tax:10116)', 'Gene') :: ['Sp3'] @entity238 :: ('7227', 'Species') :: ['Drosophila'] @entity10564 :: ('24790(Tax:10116)', 'Gene') :: ['Sp1']
@entity10564 :: (24790(Tax:10116),Gene) :: ['Sp1']
