Converts angiotensin I to angiotensin II by release of the terminal His-Leu, this results in an increase of the vasoconstrictor activity of angiotensin. Also able to inactivate bradykinin, a potent vasodilator. Has also a glycosidase activity which releases GPI-anchored proteins from the membrane by cleaving the mannose linkage in the GPI moiety. Genetic variations in ACE may be a cause of susceptibility to ischemic stroke (ISCHSTR); also known as cerebrovascular accident or cerebral infarction. A stroke is an acute neurologic event leading to death of neural tissue of the brain and resulting in loss of motor, sensory and/or cognitive function. Ischemic strokes, resulting from vascular occlusion, is considered to be a highly complex disease consisting of a group of heterogeneous disorders with multiple genetic and environmental risk factors. Defects in ACE 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). Genetic variations in ACE are associated with susceptibility to microvascular complications of diabetes type 3 (MVCD3). These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new- onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis. Defects in ACE are a cause of susceptibility to intracerebral hemorrhage (ICH). A pathological condition characterized by bleeding into one or both cerebral hemispheres including the basal ganglia and the cerebral cortex. It is often associated with hypertension and craniocerebral trauma. Intracerebral bleeding is a common cause of stroke. Belongs to the peptidase M2 family. 4 isoforms of the human protein are produced by alternative splicing. Note: This description may include information from UniProtKB.
Protein type: Protease; Membrane protein, integral; EC 22.214.171.124
Chromosomal Location of Human Ortholog: 17q23.3
Cellular Component: extracellular space; lysosome; plasma membrane; extracellular region; integral to membrane; endosome; external side of plasma membrane
Molecular Function: tripeptidyl-peptidase activity; peptidyl-dipeptidase activity; metallopeptidase activity; zinc ion binding; carboxypeptidase activity; mitogen-activated protein kinase kinase binding; drug binding; actin binding; protein binding; bradykinin receptor binding; endopeptidase activity; exopeptidase activity; mitogen-activated protein kinase binding; chloride ion binding
Biological Process: mononuclear cell proliferation; regulation of vasodilation; angiotensin mediated regulation of renal output; neutrophil mediated immunity; regulation of angiotensin metabolic process; proteolysis; angiotensin maturation; arachidonic acid secretion; regulation of systemic arterial blood pressure by renin-angiotensin; antigen processing and presentation of peptide antigen via MHC class I; regulation of smooth muscle cell migration; cellular protein metabolic process; heart contraction; regulation of vasoconstriction; peptide catabolic process; beta-amyloid metabolic process; regulation of blood pressure; angiotensin catabolic process in blood; hormone catabolic process; blood vessel remodeling; spermatogenesis; kidney development
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.