ELISA/assay

Rat Angiotensin I Converting Enzyme ELISA Kit

MBS733102

48-Strip-Wells

440 USD

ELISA Kit

Rat Angiotensin I Converting Enzyme ELISA Kit

[Angiotensin I Converting Enzyme]

[Rat Angiotensin I Converting Enzyme ELISA Kit; Angiotensin I Converting Enzyme; Angiotensin I Converting Enzyme (Rat)]

[angiotensin I converting enzyme (peptidyl-dipeptidase A) 1; 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 I]

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

ACE_HUMAN

Rat

This assay has high sensitivity and excellent specificity for detection of ACE1. No significant cross-reactivity or interference between ACE1 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between ACE1 and all the analogues, therefore, cross reaction may still exist in some cases.

Store all reagents at 2-8 degree C

Typical Testing Data/Standard Curve (for reference only)

Samples: Serum, plasma, cell culture supernatants, body fluid and tissue homogenate. Assay Type: Quantitative Competitive. Sensitivity: 1.0 pg/mL

Rat ELISA Kit

Intended Uses: This ACE1 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Rat ACE1. Principle of the Assay: ACE1 ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-ACE1 antibody and an ACE1-HRP conjugate. The assay sample and buffer are incubated together with ACE1-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 ACE1 concentration since ACE1 from samples and ACE1-HRP conjugate compete for the anti-ACE1 antibody binding site. Since the number of sites is limited, as more sites are occupied by ACE1 from the sample, fewer sites are left to bind ACE1-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The ACE1 concentration in each sample is interpolated from this standard curve.

37790804

AAR03504

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: Membrane protein, integral; EC 3.4.15.1; Protease. 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: peptidyl-dipeptidase activity; tripeptidyl-peptidase activity; zinc ion binding; carboxypeptidase activity; metallopeptidase 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; angiotensin maturation; proteolysis; 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; peptide catabolic process; beta-amyloid metabolic process; regulation of blood pressure; regulation of vasoconstriction; angiotensin catabolic process in blood; spermatogenesis; blood vessel remodeling; hormone catabolic process; kidney development. Disease: Renal Tubular Dysgenesis; Microvascular Complications Of Diabetes, Susceptibility To, 3; Alzheimer Disease; Hemorrhage, Intracerebral, Susceptibility To

48-Strip-Wells

440 USD

96-Strip-Wells

640

5x96-Strip-Wells

2895

10x96-Strip-Wells

5415