ELISA/assay

Rat Angiotensin I Converting Enzyme ELISA Kit

MBS019517

48-Strip-Wells

435 USD

ELISA Kit

Rat Angiotensin I Converting Enzyme ELISA Kit

Angiotensin I Converting Enzyme

angiotensin I converting enzyme; Angiotensin-converting enzyme; angiotensin-converting enzyme; kininase II; peptidase P; CD143 antigen; testicular ECA; carboxycathepsin; dipeptidyl carboxypeptidase 1; dipeptidyl carboxypeptidase I; angiotensin converting enzyme, somatic isoform; angiotensin I converting enzyme (peptidyl-dipeptidase A) 1; angiotensin I converting enzyme peptidyl-dipeptidase A 1 transcript; angiotensin I converting enzyme; Dipeptidyl carboxypeptidase I; Kininase II

ACE

ACE; ACE; DCP; ICH; ACE1; DCP1; CD143; MVCD3; DCP; DCP1; ACE

ACE_HUMAN

Rat

No significant cross-reactivity or interference between Rat ACE and analogues was observed.

Store all reagents at 2-8 degree C

Samples: Serum, Plasma, Tissue Homogenate, Feces and Urine. Assay Type: Sandwich. Detection Range: 6.25 U/L - 200 U/L. Sensitivity: 1.0 U/L.

Intended Uses: This Quantitative Sandwich ELISA kit is only for in vitro research use only, not for drug, household, therapeutic or diagnostic applications! It is intended to be determinated ACE concentrations in Rat serum, plasma and other body fluids. Using Purified Rat ACE antibody to coat Microelisa Stripplate wells to make solid-phase antibody, then add ACE and ACE antibody which has been labeled with HRP to wells, then the reactants become antibody-antigen-antibody-enzyme complex, after washing completely, add TMB substrate solution, TMB substrate becomes blue color under HRP enzyme-catalyzed, reaction is terminated by the addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm. The concentration of ACE in the samples is then determined by comparing the O.D. of the samples to the standard curve. Intra-assay Precision: Intra-assay CV (%) is less than 15%. Inter-assay Precision: Inter-assay CV (%) is less than 15%. [CV(%) = SD/mean ×100]

Background: This Quantitative Sandwich ELISA kit is only for in vitro research use only, not for drug, household, therapeutic or diagnostic applications! It is intended to be determinated ACE concentrations in Rat serum, plasma and other body fluids. Using Purified Rat ACE antibody to coat Microelisa Stripplate wells to make solid-phase antibody, then add ACE and ACE antibody which has been labeled with HRP to wells, then the reactants become antibody-antigen-antibody-enzyme complex, after washing completely, add TMB substrate solution, TMB substrate becomes blue color under HRP enzyme-catalyzed, reaction is terminated by the addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm. The concentration of ACE in the samples is then determined by comparing the O.D. of the samples to the standard curve.

76057114

ABA39229.1

P12821

149,715 Da

ACE Inhibitor Pathway (198763); Chagas Disease (American Trypanosomiasis) Pathway (147809); Chagas Disease (American Trypanosomiasis) Pathway (147795); Hypertrophic Cardiomyopathy (HCM) Pathway (114229); Hypertrophic Cardiomyopathy (HCM) Pathway (106591); Metabolism Of Angiotensinogen To Angiotensins Pathway (685555); Metabolism Of Proteins Pathway (106230); Peptide Hormone Metabolism Pathway (771603); Renin-angiotensin System Pathway (83075); Renin-angiotensin System Pathway (486)

This gene encodes an enzyme involved in catalyzing the conversion of angiotensin I into a physiologically active peptide angiotensin II. Angiotensin II is a potent vasopressor and aldosterone-stimulating peptide that controls blood pressure and fluid-electrolyte balance. This enzyme plays a key role in the renin-angiotensin system. Many studies have associated the presence or absence of a 287 bp Alu repeat element in this gene with the levels of circulating enzyme or cardiovascular pathophysiologies. Multiple alternatively spliced transcript variants encoding different isoforms have been identified, and two most abundant spliced variants encode the somatic form and the testicular form, respectively, that are equally active. [provided by RefSeq, May 2010]

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; EC 3.4.15.1; Membrane protein, integral. Chromosomal Location of Human Ortholog: 17q23.3. Cellular Component: extracellular space; lysosome; integral to membrane; plasma membrane; extracellular region; endosome; external side of plasma membrane. Molecular Function: tripeptidyl-peptidase activity; peptidyl-dipeptidase activity; zinc ion binding; metallopeptidase activity; 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; neutrophil mediated immunity; angiotensin mediated regulation of renal output; regulation of angiotensin metabolic process; arachidonic acid secretion; angiotensin maturation; proteolysis; regulation of systemic arterial blood pressure by renin-angiotensin; antigen processing and presentation of peptide antigen via MHC class I; cellular protein metabolic process; regulation of smooth muscle cell migration; heart contraction; peptide catabolic process; regulation of vasoconstriction; regulation of blood pressure; beta-amyloid metabolic process; angiotensin catabolic process in blood; blood vessel remodeling; hormone catabolic process; spermatogenesis; kidney development. Disease: Microvascular Complications Of Diabetes, Susceptibility To, 3; Renal Tubular Dysgenesis; Alzheimer Disease; Hemorrhage, Intracerebral, Susceptibility To

48-Strip-Wells

435 USD

96-Strip-Wells

600