Human Angiotensin 1-7 ELISA Kit
Human Angiotensin 1-7 ELISA Kit for ELISA and Human
Cancer kit; Cell Biology and Cellular Response kit; Metabolism kit
ARG80960 Human Angiotensin 1-7 ELISA Kit is an Enzyme Immunoassay kit for the quantification of Human Angiotensin 1-7 in cell culture supernatant, serum, plasma and other suitable sample solution.
|Target Name||Angiotensin 1-7|
|Sample Type||Cell culture supernatant, serum, plasma and other suitable sample solution.|
|Standard Range||15.6 - 500 pg/ml|
|Sample Volume||100 µl|
|Full Name||angiotensinogen (serpin peptidase inhibitor, clade A, member 8)|
|Alternate Names||Des-Asp-angiotensin II; Angiotensin III; SERPINA8; Angiotensinogen; Angiotensin 3-8; Ang IV; Ang I; Angiotensin I; Angiotensin II; Angiotensin 1-8; Angiotensin 1-10; Angiotensin IV; Ang III; Ang II; Angiotensin 2-8; ANHU; Serpin A8|
|Assay Time||90 min|
|Storage instruction||Store the kit at 2-8°C. Keep microplate wells sealed in a dry bag with desiccants. Do not expose test reagents to heat, sun or strong light during storage and usage. Please refer to the product user manual for detail temperatures of the components.|
|Note||For laboratory research only, not for drug, diagnostic or other use.|
|Gene Full Name||angiotensinogen (serpin peptidase inhibitor, clade A, member 8)|
|Background||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]|
|Function||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. [UniProt]
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|Research Area||Cancer kit; Cell Biology and Cellular Response kit; Metabolism kit|
|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.
In response to low blood pressure, the enzyme renin/REN cleaves angiotensinogen to produce angiotensin-1. Angiotensin-1 is a substrate of ACE (angiotensin converting enzyme) that removes a dipeptide to yield the physiologically active peptide angiotensin-2. Angiotensin-1 and angiotensin-2 can be further processed to generate angiotensin-3, angiotensin-4. Angiotensin 1-9 is cleaved from angiotensin-1 by ACE2 and can be further processed by ACE to produce angiotensin 1-7, angiotensin 1-5 and angiotensin 1-4. Angiotensin 1-7 has also been proposed to be cleaved from angiotensin-2 by ACE2 or from angiotensin-1 by MME (neprilysin).
The disulfide bond is labile. Angiotensinogen is present in the circulation in a near 40:60 ratio with the oxidized disulfide-bonded form, which preferentially interacts with receptor-bound renin.
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|ARG80960 Human Angiotensin 1-7 ELISA Kit User's manual||Download|