Activation of gastrin gene transcription in islet cells by a RAP1-like cis-acting promoter element.
Gastrin transcription in islet cells is activated by a cis-regulatory sequence containing a binding site for the yeast transcription factor RAP1. The DNA-protein interactions between RAP1 protein and the gastrin DNA element determined by methylation interference assays are identical to those of RAP1 and yeast genes. Point mutations in the gastrin RAP1 binding site, which abolished RAP1 binding, decreased transcriptional activation by this sequence. Islet cells revealed a DNA binding protein with RAP1-like binding specificity. These findings support the conclusion that gastrin transcription is activated in mammalian cells by a RAP1-like transcription factor.
Simon
B
B
Massachusetts General Hospital, Department of Medicine, Harvard Medical School, Boston 02114.
Tillotson
L
L
Brand
S J
SJ
D000818:Animals; D001483:Base Sequence; D002460:Cell Line; D006224:Cricetinae; D004247:DNA / Q000378:metabolism; D019204:GTP-Binding Proteins / Q000378:metabolism*; D005755:Gastrins / Q000235:genetics*; D006801:Humans; D007515:Islets of Langerhans / Q000166:cytology / Q000378:metabolism*; D008969:Molecular Sequence Data; D011401:Promoter Regions, Genetic; D051381:Rats; D012689:Sequence Homology, Nucleic Acid; D014157:Transcription Factors / Q000378:metabolism*; D014158:Transcription, Genetic; D014407:Tumor Cells, Cultured; D020668:rap GTP-Binding Proteins
D005755:Gastrins; D014157:Transcription Factors; D004247:DNA; D019204:GTP-Binding Proteins; D020668:rap GTP-Binding Proteins