ELISA/assay

Human Angiotensin I Converting Enzyme ELISA Kit

MBS727096

48-Strip-Wells

440 USD

ELISA Kit

Human Angiotensin I Converting Enzyme ELISA Kit

[Angiotensin I Converting Enzyme]

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

[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

Human

This assay has high sensitivity and excellent specificity for detection of ACCN3. No significant cross-reactivity or interference between ACCN3 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between ACCN3 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: 0.1 ng/mL.

Human ELISA Kit

Intended Uses: This ACCN3 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Human ACCN3. This ELISA kit for research use only, not for therapeutic or diagnostic applications!. Principle of the Assay: ACCN3 ELISA kit applies the competitive enzyme immunoassay technique utilizing an anti-ACCN3 antibody and an ACCN3-HRP conjugate. The assay sample and buffer are incubated together with ACCN3-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 ACCN3 concentration since ACCN3 from samples and ACCN3-HRP conjugate compete for the anti-ACCN3 antibody binding site. Since the number of sites is limited, as more sites are occupied by ACCN3 from the sample, fewer sites are left to bind ACCN3-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The ACCN3 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]

Function: 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. Catalytic activity: Release of a C-terminal dipeptide, oligopeptide- -Xaa-Yaa, when Xaa is not Pro, and Yaa is neither Asp nor Glu. Thus, conversion of angiotensin I to angiotensin II, with increase in vasoconstrictor activity, but no action on angiotensin II. Cofactor: Binds 2 zinc ions per subunit. Isoform Testis-specific only binds 1 zinc ion per subunit.Binds 3 chloride ions per subunit. Enzyme regulation: Strongly activated by chloride. Specifically inhibited by lisinopril, captopril and enalaprilat. Subcellular location: Angiotensin-converting enzyme, soluble form: Secreted. Cell membrane; Single-pass type I membrane protein. Tissue specificity: Ubiquitously expressed, with highest levels in lung, kidney, heart, gastrointestinal system and prostate. Isoform Testis-specific is expressed in spermatocytes and adult testis. Ref.15 Ref.16 Ref.19 Ref.22. Induction: Up-regulated in failing heart. Ref.21 Ref.22. Post-translational modification: Phosphorylated by CK2 on Ser-1299; which allows membrane retention. Ref.18. Involvement in disease: Ischemic stroke (ISCHSTR) [MIM:601367]: 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.Note: Disease susceptibility is associated with variations affecting the gene represented in this entry. Ref.33Renal tubular dysgenesis (RTD) [MIM:267430]: 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).Note: The disease is caused by mutations affecting the gene represented in this entry. Ref.35Microvascular complications of diabetes 3 (MVCD3) [MIM:612624]: 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.Note: Disease susceptibility is associated with variations affecting the gene represented in this entry.Intracerebral hemorrhage (ICH) [MIM:614519]: 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.Note: Disease susceptibility is associated with variations affecting the gene represented in this entry. Ref.34. Miscellaneous: Inhibitors of ACE are commonly used to treat hypertension and some types of renal and cardiac dysfunction.The glycosidase activity probably uses different active site residues than the metalloprotease activity. Sequence similarities: Belongs to the peptidase M2 family. Biophysicochemical propertiesKinetic parameters:KM=2.51 mM for Hip-His-Leu Ref.17 Ref.20. Sequence caution: The sequence BAD92208.1 differs from that shown. Reason: Erroneous initiation.

48-Strip-Wells

440 USD

96-Strip-Wells

640

5x96-Strip-Wells

2895

10x96-Strip-Wells

5415