Aliases for AGT Gene
External Ids for AGT Gene
Previous HGNC Symbols for AGT Gene
Previous GeneCards Identifiers for AGT Gene
The protein encoded by this gene, pre-angiotensinogen or angiotensinogen precursor, is expressed in the liver and is cleaved by the enzyme renin in response to lowered blood pressure. The resulting product, angiotensin I, is then cleaved by angiotensin converting enzyme (ACE) to generate the physiologically active enzyme angiotensin II. The protein is involved in maintaining blood pressure and in the pathogenesis of essential hypertension and preeclampsia. Mutations in this gene are associated with susceptibility to essential hypertension, and can cause renal tubular dysgenesis, a severe disorder of renal tubular development. Defects in this gene have also been associated with non-familial structural atrial fibrillation, and inflammatory bowel disease. [provided by RefSeq, Jul 2008]
GeneCards Summary for AGT Gene
AGT (Angiotensinogen) is a Protein Coding gene. Diseases associated with AGT include Renal Tubular Dysgenesis and Hypertension, Essential. Among its related pathways are Peptide ligand-binding receptors and RET signaling. GO annotations related to this gene include growth factor activity and serine-type endopeptidase inhibitor activity. An important paralog of this gene is SERPINH1.
UniProtKB/Swiss-Prot for AGT Gene
Essential component of the renin-angiotensin system (RAS), a potent regulator of blood pressure, body fluid and electrolyte homeostasis.
Angiotensin-2: acts directly on vascular smooth muscle as a potent vasoconstrictor, affects cardiac contractility and heart rate through its action on the sympathetic nervous system, and alters renal sodium and water absorption through its ability to stimulate the zona glomerulosa cells of the adrenal cortex to synthesize and secrete aldosterone.
Angiotensin-3: stimulates aldosterone release.
Angiotensin 1-7: is a ligand for the G-protein coupled receptor MAS1. Has vasodilator and antidiuretic effects. Has an antithrombotic effect that involves MAS1-mediated release of nitric oxide from platelets.