ACE ELISA Kit for Mouse

ACE: 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.

Protein type: Protease; Membrane protein, integral; EC 3.4.15.1

Cellular Component: extracellular space; membrane; brush border membrane; lysosome; cytoplasm; plasma membrane; integral to membrane; basal plasma membrane; extracellular region; endosome; vesicle; external side of plasma membrane

Molecular Function: metallopeptidase activity; carboxypeptidase activity; zinc ion binding; mitogen-activated protein kinase kinase binding; mannosyl-oligosaccharide mannosidase activity; metal ion binding; drug binding; actin binding; glucosidase activity; endopeptidase activity; mitogen-activated protein kinase binding; amylase activity; chloride ion binding; peptidyl-dipeptidase activity; tripeptidyl-peptidase activity; hydrolase activity; trehalase activity; peptidase activity; protein binding; fucosidase activity; hexosaminidase activity; lytic transglycosylase activity; galactosidase activity; bradykinin receptor binding; exopeptidase activity; mannosidase activity

Biological Process: positive regulation of protein binding; positive regulation of apoptosis; neutrophil mediated immunity; response to lipopolysaccharide; positive regulation of systemic arterial blood pressure; regulation of angiotensin metabolic process; proteolysis; sensory perception of pain; peptide metabolic process; regulation of smooth muscle cell migration; peptide catabolic process; beta-amyloid metabolic process; regulation of blood pressure; kidney development; negative regulation of protein binding; vasoconstriction; positive regulation of neurogenesis; organ regeneration; eating behavior; arachidonic acid secretion; regulation of systemic arterial blood pressure by renin-angiotensin; heart contraction; spermatogenesis; hormone catabolic process; alveolus development; positive regulation of inflammatory response