ELISA/assay

Human Angiotensinogen ELISA Kit

MBS726474

48-Strip-Wells-(Comp

470 USD

ELISA Kit

Human Angiotensinogen ELISA Kit

Angiotensinogen

angiotensinogen; Angiotensinogen; angiotensinogen; serpin A8; angiotensin I; angiotensin II; pre-angiotensinogen; alpha-1 antiproteinase, antitrypsin; serine (or cysteine) proteinase inhibitor; angiotensinogen (serpin peptidase inhibitor, clade A, member 8); Serpin A8Cleaved into the following 8 chains:Angiotensin-1Alternative name(s):Angiotensin 1-10; Angiotensin I; Ang I

AGT

AGT; AGT; ANHU; SERPINA8; SERPINA8; Ang I; Ang II; Ang III; Ang IV

ANGT_HUMAN

Human

This assay has high sensitivity and excellent specificity for detection of AGT. No significant cross-reactivity or interference between AGT and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between AGT and all the analogues, therefore, cross reaction may still exist in some cases.

Store all reagents at 2-8 degree C.

Assay Type: Competitive or Sandwich. Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate. Sensitivity: 0.1 ng/mL.

Intended Uses: This AGT ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Human AGT. This ELISA kit for research use only, not for therapeutic or diagnostic applications!

Cardiovascular

Principle of the assay: AGT ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-AGT antibody and an AGT-HRP conjugate. The assay sample and buffer are incubated together with AGT-HRP conjugate in pre-coated plate for one hour. After the incubation period, the wells are decanted and washed five times. The wells are then incubated with a substrate for HRP enzyme. The product of the enzyme-substrate reaction forms a blue colored complex. Finally, a stop solution is added to stop the reaction, which will then turn the solution yellow. The intensity of color is measured spectrophotometrically at 450nm in a microplate reader. The intensity of the color is inversely proportional to the AGT concentration since AGT from samples and AGT-HRP conjugate compete for the anti-AGT antibody binding site. Since the number of sites is limited, as more sites are occupied by AGT from the sample, fewer sites are left to bind AGT-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The AGT concentration in each sample is interpolated from this standard curve.

532198

AAA51679.1

53,154 Da

ACE Inhibitor Pathway (198763); Adipogenesis Pathway (198832); Class A/1 (Rhodopsin-like Receptors) Pathway (106357); Fatty Acid, Triacylglycerol, And Ketone Body Metabolism Pathway (160977); G Alpha (i) Signalling Events Pathway (119550); G Alpha (q) Signalling Events Pathway (106043); GPCR Downstream Signaling Pathway (119548); GPCR Ligand Binding Pathway (161020); Gastrin-CREB Signalling Pathway Via PKC And MAPK (645295); Metabolism Pathway (477135)

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]

angiotensin: 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. Protein type: Secreted; Secreted, signal peptide. Chromosomal Location of Human Ortholog: 1q42.2. Cellular Component: extracellular space; cytoplasm; extracellular region. Molecular Function: serine-type endopeptidase inhibitor activity; protein binding; sodium channel regulator activity; growth factor activity; hormone activity; superoxide-generating NADPH oxidase activator activity; type 2 angiotensin receptor binding; type 1 angiotensin receptor binding. Biological Process: extracellular matrix organization and biogenesis; renal system process; positive regulation of nitric oxide biosynthetic 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; female pregnancy; positive regulation of multicellular organism growth; positive regulation of vasodilation; 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; regulation of calcium ion transport; response to muscle activity involved in regulation of muscle adaptation; 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 transmission of nerve impulse; regulation of vasoconstriction; 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; positive regulation of cellular protein metabolic process; renin-angiotensin regulation of aldosterone production; 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; regulation of blood pressure; 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; positive regulation of peptidyl-serine phosphorylation; 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; negative regulation of cell growth; response to cold; astrocyte activation; positive regulation of inflammatory response. Disease: Renal Tubular Dysgenesis; Hypertension, Essential

48-Strip-Wells-(Competitive)

470 USD

48-Strip-Wells-(Sandwich)

470

96-Strip-Wells-(Competitive)

675

96-Strip-Wells-(Sandwich)

675