Essential component of the renin-angiotensin system (RAS), a potent regulator of blood pressure, body fluid and electrolyte homeostasis. In response to lowered blood pressure, the enzyme renin cleaves angiotensinogen to produce angiotensin-1 (angiotensin 1-10). Angiotensin-1 is a substrate of ACE (angiotensin converting enzyme) that removes a dipeptide to yield the physiologically active peptide angiotensin-2 (angiotensin 1- 8). Angiotensin-1 and angiotensin-2 can be further processed to generate angiotensin-3 (angiotensin 2-8), angiotensin-4 (angiotensin 3-8). Angiotensin 1-7 is cleaved from angiotensin-2 by ACE2 or from angiotensin-1 by MME (neprilysin). Angiotensin 1-9 is cleaved from angiotensin-1 by ACE2. Genetic variations in AGT are a cause of susceptibility to essential hypertension (EHT). Essential hypertension is a condition in which blood pressure is consistently higher than normal with no identifiable cause. Defects in AGT are a cause of renal tubular dysgenesis (RTD). RTD is an autosomal recessive severe disorder of renal tubular development characterized by persistent fetal anuria and perinatal death, probably due to pulmonary hypoplasia from early-onset oligohydramnios (the Potter phenotype). Belongs to the serpin family. Note: This description may include information from UniProtKB.
Protein type: Secreted, signal peptide; Secreted
Chromosomal Location of Human Ortholog: 1q42.2
Cellular Component: extracellular space; extracellular region
Molecular Function: serine-type endopeptidase inhibitor activity; protein binding; growth factor activity; hormone activity; type 2 angiotensin receptor binding; type 1 angiotensin receptor binding
Biological Process: extracellular matrix organization and biogenesis; renal system process; establishment of blood-nerve barrier; negative regulation of nerve growth factor receptor signaling pathway; positive regulation of transcription, DNA-dependent; stress-activated MAPK cascade; positive regulation of multicellular organism growth; ovarian follicle rupture; activation of NF-kappaB transcription factor; positive regulation of fibroblast proliferation; cell-cell signaling; positive regulation of superoxide release; negative regulation of neuron apoptosis; kidney development; positive regulation of NAD(P)H oxidase activity; positive regulation of cytokine production; angiotensin mediated regulation of renal output; response to muscle activity involved in regulation of muscle adaptation; regulation of calcium ion transport; regulation of norepinephrine secretion; positive regulation of phosphoinositide 3-kinase cascade; negative regulation of tissue remodeling; positive regulation of peptidyl-tyrosine phosphorylation; angiotensin mediated vasoconstriction involved in regulation of systemic arterial blood pressure; phospholipase C activation; regulation of vasoconstriction; regulation of proteolysis; G-protein signaling, coupled to IP3 second messenger (phospholipase C activating); smooth muscle cell differentiation; cytokine secretion; nitric oxide mediated signal transduction; regulation of long-term neuronal synaptic plasticity; peristalsis; cell-matrix adhesion; renin-angiotensin regulation of aldosterone production; positive regulation of cellular protein metabolic process; smooth muscle cell proliferation; cellular lipid metabolic process; angiotensin maturation; excretion; vasodilation; response to salt stress; negative regulation of cell proliferation; positive regulation of MAPKKK cascade; fibroblast proliferation; renin-angiotensin regulation of blood vessel size; positive regulation of epidermal growth factor receptor signaling pathway; renin-angiotensin regulation of blood volume; regulation of cell growth; angiotensin mediated drinking behavior; artery smooth muscle contraction; aging; blood vessel development; positive regulation of fatty acid biosynthetic process; cellular sodium ion homeostasis; renal response to blood flow during renin-angiotensin regulation of systemic arterial blood pressure; activation of NF-kappaB-inducing kinase; positive regulation of organ growth; regulation of cell proliferation; G-protein coupled receptor protein signaling pathway; negative regulation of angiogenesis; cellular protein metabolic process; ureteric bud branching; blood vessel remodeling; G-protein signaling, coupled to cGMP nucleotide second messenger; response to cold; negative regulation of cell growth; astrocyte activation; positive regulation of inflammatory response
SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.