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Publication : Molecular dissection of mouse soluble guanylyl cyclase alpha1 promoter.

First Author  Vazquez-Padron RI Year  2004
Journal  Biochem Biophys Res Commun Volume  314
Issue  1 Pages  208-14
PubMed ID  14715267 Mgi Jnum  J:87713
Mgi Id  MGI:3027454 Doi  10.1016/j.bbrc.2003.12.078
Citation  Vazquez-Padron RI, et al. (2004) Molecular dissection of mouse soluble guanylyl cyclase alpha1 promoter. Biochem Biophys Res Commun 314(1):208-14
abstractText  Soluble guanylyl cyclase (sGC) is the only known receptor for nitric oxide (NO) and is downregulated in aging and hypertension. Little is known about sGC gene transcriptional regulation. In order to characterize the sGC transcriptional system, we cloned and sequenced the 5(') flanking region of mouse sGC alpha(1) gene (AY116663). Structurally, it is a non-canonical TATA-less promoter that we mapped to chromosome 3 with many putative regulation sites for Sp-1, NF-kappaB, and AP-1 transcription factors amongst others, and two (TG:CA)(n) dinucleotide microsatellites near the transcriptional start point. The cloned upstream sequence produced a 5-fold increase in luciferase activity in Cos7, HeLa, NIH3T3, and 293 cells as well as in mouse VSMC-like kidney mesangial cells. In the latter cell type, we showed that sGC alpha(1) promoter activity was dependent on the presence of its 5(') unstranslated region (5(')UTR).
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