Caution:It is uncertain whether Met-1 or Met-10 is the initiator.,Disease:Defects in AGT are a cause of renal tubular dysgenesis (RTD) [MIM:267430]. 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).,Disease:Defects in AGT are associated with susceptibility to essential hypertension [MIM:145500]. Hypertension also occurs in 5-7% of all pregnancies where it is a leading cause of maternal, fetal and neonatal morbidity and mortality. Among pregnancy-induced hypertension cases, severe pre-eclampsia [MIM:189800] is characterized by the development of hypertension and proteinuria after the 20th week of pregnancy and is the most distinctive, life-threatening form.,Function:Angiotensin-3 stimulates aldosterone release.,Function:In response to lowered blood pressure, the enzyme renin cleaves angiotensin-1, from angiotensinogen. ACE (angiotensin converting enzyme) then removes a dipeptide to yield the physiologically active peptide angiotensin-2, the most potent pressor substance known, which helps regulate volume and mineral balance of body fluids.,online information:Angiotensin entry,online information:The Singapore human mutation and polymorphism database,PTM:Beta-decarboxylation of Asp-34 in angiotensin-2, by mononuclear leukocytes produces alanine. The resulting peptide form, angiotensin-A, has the same affinity for the AT1 receptor as angiotensin-2, but a higher affinity for the AT2 receptor.,similarity:Belongs to the serpin family.,subunit:During pregnancy, exists as a disulfide-linked 2:2 heterotetramer with the proform of PRG2 and as a complex (probably a 2:2:2 heterohexamer) with pro-PRG2 and C3dg.,tissue specificity:Expressed by the liver and secreted in plasma.,
展开内容