The mouse gene for the inducible G-protein-coupled receptoredg-1

CH Liu, T Hla - Genomics, 1997 - Elsevier
CH Liu, T Hla
Genomics, 1997Elsevier
Edg-1, an immediate-early gene induced during thein vitrodifferentiation of human
endothelial cells, encodes a G-protein-coupled receptor (GPR) that signals via the
Gi/mitogen-activated protein kinase (MAP kinase) pathway (Lee, M.-J., Evans, M., and Hla,
T.(1996) J. Biol. Chem. 271, 11272–11279). It is a prototypical member of the subfamily of
“orphan” receptors that are expressed in the cardiovascular and nervous systems. In this
report, the mouseedg-1gene was cloned and sequenced, and its expression patterns were …
Edg-1,an immediate-early gene induced during thein vitrodifferentiation of human endothelial cells, encodes a G-protein-coupled receptor (GPR) that signals via the Gi/mitogen-activated protein kinase (MAP kinase) pathway (Lee, M.-J., Evans, M., and Hla, T. (1996)J. Biol. Chem.271, 11272–11279). It is a prototypical member of the subfamily of “orphan” receptors that are expressed in the cardiovascular and nervous systems. In this report, the mouseedg-1gene was cloned and sequenced, and its expression patterns were defined. Theedg-1transcript was expressed in a wide variety of adult tissues including the brain, lung, liver, heart, and spleen. However, during embryogenesis, theedg-1mRNA was induced late in development (after Embryonic Day 15.5) at centers of ossification. As a first step toward understanding the molecular basis of tissue-specific and inducible expression, the mouseedg-1gene and its promoter were characterized. The mouseedg-1gene is composed of two exons and is 4.9 kb in length. The second exon is large and contains the entire coding region and the 3′-untranslated region. Theedg-1promoter is TATA-less and contains GC-rich elements, and transcription initiation occurs from a single start site. The 5′-flanking region of the promoter contains several enhancer elements. However, the activity of the 5′-flanking region was suppressed by the repressor activity within the first intron. These data provide the basis for the further characterization of the regulation of the orphan GPRedg-1.
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