For Research Use Only. Not for use in diagnostic procedures.

Store all reagents at 2-8 degree C.

We suggest pre-experimenting with neat (undiluted) samples, 1:2 or 1:4 dilutions. Please avoid diluting your samples more than 1:10 as it would exceed the dilution limit set for this kit. If the expected concentration of the target is beyond the detection range of the kit, please contact our technical support team

Select online data sheet information is drawn from bioinformatics databases, occasionally resulting in ambiguous or non-relevant product information. It is the responsibility of the customer to review, verify, and evaluate the information to make sure it matches their requirements before purchasing the kit. Our ELISA Kit assays are dynamic research tools and sometimes they may be updated and improved. If the format of this assay is important to you then please request the current manual or contact our technical support team with a presales inquiry before placing an order. We will confirm the current details of the assay. We cannot guarantee the sample manual posted online is the most current manual.

Small volumes of ELN elisa kit vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

MBS740397 is a ready-to-use microwell, strip plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the Elastin (ELN) ELISA Kit target analytes in biological samples. The concentration gradients of the kit standards or positive controls render a theoretical kit detection range in biological research samples containing ELN. The ELISA analytical biochemical technique of the MBS740397 kit is based on ELN antibody-ELN antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect ELN antigen targets in samples. The ELISA Kit is designed to detect native, not recombinant, ELN. Appropriate sample types may include undiluted body fluids and/or tissue homogenates, secretions. Quality control assays assessing reproducibility identified the intra-assay CV (%) and inter-assay CV(%).

Principle of the Assay: ELN ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-ELN antibody and an ELN-HRP conjugate. The assay sample and buffer are incubated together with ELN-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 ELN concentration since ELN from samples and ELN-HRP conjugate compete for the anti-ELN antibody . Since the number of sites is limited, as more sites are occupied by ELN from the sample, fewer sites are left to bind ELN-HRP conjugate. 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.

Cell Biology

60,980 Da

elastin

elastin; tropoelastin

Elastin

ELN_HUMAN

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; Secreted, signal peptide; Extracellular matrix

Chromosomal Location of Human Ortholog: 7q11.23

Cellular Component: proteinaceous extracellular matrix; extracellular region

Molecular Function: protein binding; extracellular matrix structural constituent

Biological Process: extracellular matrix disassembly; cell proliferation; organ morphogenesis; extracellular matrix organization and biogenesis; blood circulation; respiratory gaseous exchange

Disease: Cutis Laxa, Autosomal Dominant 1; Williams-beuren Syndrome; Supravalvular Aortic Stenosis

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