ELISA/assay

Mouse Elastin ELISA Kit

MBS728941

48-Strip-Wells

470 USD

ELISA Kit

Mouse Elastin ELISA Kit

Elastin

elastin; Elastin; elastin; tropoelastin; elastin; Tropoelastin

ELN

ELN; ELN; WS; WBS; SVAS

ELN_HUMAN

Mouse

Store all reagents at 2-8 degree C.

Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate. Assay Type: Sandwich

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

Cell Biology

Principle of the Assay: ELN ELISA kit applies the quantitative sandwich enzyme immunoassay technique. The microtiter plate has been pre-coated with a monoclonal antibody specific for ELN. Standards or samples are then added to the microtiter plate wells and ELN if present, will bind to the antibody pre-coated wells. In order to quantitatively determine the amount of ELN present in the sample, a standardized preparation of horseradish peroxidase (HRP)-conjugated polyclonal antibody, specific for ELN are added to each well to "sandwich" the ELN immobilized on the plate. The microtiter plate undergoes incubation, and then the wells are thoroughly washed to remove all unbound components. Next, substrate solutions are added to each well. The enzyme (HRP) and substrate are allowed to react over a short incubation period. Only those wells that contain ELN and enzyme-conjugated antibody will exhibit a change in color. The enzyme-substrate reaction is terminated by addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The ELN concentration in each sample is interpolated from this standard curve.

182021

AAC98395.1

60,980 Da

Elastic Fibre Formation Pathway (730310); Extracellular Matrix Organization Pathway (576262); Protein Digestion And Absorption Pathway (172847); Protein Digestion And Absorption Pathway (171868)

This gene encodes a protein that is one of the two components of elastic fibers. The encoded protein is rich in hydrophobic amino acids such as glycine and proline, which form mobile hydrophobic regions bounded by crosslinks between lysine residues. Deletions and mutations in this gene are associated with supravalvular aortic stenosis (SVAS) and autosomal dominant cutis laxa. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008]

elastin: Major structural protein of tissues such as aorta and nuchal ligament, which must expand rapidly and recover completely. Molecular determinant of the late arterial morphogenesis, stabilizing arterial structure by regulating proliferation and organization of vascular smooth muscle. Defects in ELN are the cause of cutis laxa, autosomal dominant, type 1 (ADCL1). A connective tissue disorder characterized by loose, hyperextensible skin with decreased resilience and elasticity leading to a premature aged appearance. Face, hands, feet, joints, and torso may be differentially affected. Additional variable clinical features are gastrointestinal diverticula, hernia, and genital prolapse. Rare manifestations are pulmonary artery stenosis, aortic aneurysm, bronchiectasis, and emphysema. Defects in ELN are the cause of supravalvular aortic stenosis (SVAS). SVAS is a congenital narrowing of the ascending aorta which can occur sporadically, as an autosomal dominant condition, or as one component of Williams-Beuren syndrome. ELN is located in the Williams-Beuren syndrome (WBS) critical region. WBS results from a hemizygous deletion of several genes on chromosome 7q11.23, thought to arise as a consequence of unequal crossing over between highly homologous low-copy repeat sequences flanking the deleted region. Haploinsufficiency of ELN may be the cause of certain cardiovascular and musculo-skeletal abnormalities observed in the disease. Belongs to the elastin family. 13 isoforms of the human protein are produced by alternative splicing. Protein type: Secreted; Extracellular matrix; Secreted, signal peptide. Chromosomal Location of Human Ortholog: 7q11.23. Cellular Component: proteinaceous extracellular matrix; extracellular region. Molecular Function: protein binding; extracellular matrix structural constituent. Biological Process: cell proliferation; extracellular matrix disassembly; extracellular matrix organization and biogenesis; organ morphogenesis; blood circulation; respiratory gaseous exchange. Disease: Cutis Laxa, Autosomal Dominant 1; Williams-beuren Syndrome; Supravalvular Aortic Stenosis

48-Strip-Wells

470 USD

96-Strip-Wells

675