GO curators for mouse genes have assigned the following annotations to the gene product of Ren1. (This text reflects annotations as of Wednesday, January 23, 2013.) Summary from NCBI RefSeq
[Summary is not available for the mouse gene. This summary is for the human ortholog.] Renin catalyzes the first step in the activation pathway of angiotensinogen--a cascade that can result in aldosterone release,vasoconstriction, and increase in blood pressure. Renin, an aspartyl protease, cleaves angiotensinogen to form angiotensin I, which is converted to angiotensin II by angiotensin I converting enzyme, an important regulator of blood pressure and electrolyte balance. Transcript variants that encode different protein isoforms and that arise from alternative splicing and the use of alternative promoters have been described, but their full-length nature has not been determined. Mutations in this gene have been shown to cause familial hyperproreninemia. [provided by RefSeq, Jul 2008]Summary text based on GO annotations supported by experimental evidence in mouse
Researchers have inferred from direct assay, that the gene product of Ren1
participates in the following biological processes:
Fowler JD et al. (2009) Regulated renin release from 3T3-L1 adipocytes. Am J Physiol Endocrinol Metab, 296:E1383-91. (PubMed:19293336)
Kim HS et al. (1999) Homeostasis in mice with genetically decreased angiotensinogen is primarily by an increased number of renin-producing cells. J Biol Chem, 274:14210-7. (PubMed:10318840)
Klar J et al. (2004) Aldosterone enhances renin gene expression in juxtaglomerular cells. Am J Physiol Renal Physiol, 286:F349-55. (PubMed:14583438)
Yanai K et al. (2000) Renin-dependent cardiovascular functions and renin-independent blood-brain barrier functions revealed by renin-deficient mice. J Biol Chem, 275:5-8. (PubMed:10617578)