Collagen alpha-1(III) chain; COL3A1

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

This assay recognizes recombinant and natural human collagen alpha-1 (III) chain. No significant cross-reactivity or interference was observed.

For long term storage, please store the entire kit at -20 degree C.

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Small volumes of COL3A1 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.

MBS2880513 is a ready-to-use microwell, strip plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the Collagen alpha-1(III) chain (COL3A1) 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 COL3A1. The ELISA analytical biochemical technique of the MBS2880513 kit is based on COL3A1 antibody-COL3A1 antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect COL3A1 antigen targets in samples. The ELISA Kit is designed to detect native, not recombinant, COL3A1. 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(%).

Intended Uses: This immunoassay kit allows for the in vitro quantitative determination of human collagen alpha-1 (iii) chain, collagen alpha-1 (III) chain concentrations in serum, Plasma, Urine, tissue homogenates and Cell culture supernates and Other biological fluids.

Principle of the Assay: The microtiter plate provided in this kit has been pre-coated with an antibody specific to Collagen alpha-1(III) chain. Standards or samples are then added to the appropriate microtiter plate wells with a biotin-conjugated antibody preparation specific for Collagen alpha-1(III) chain and Avidin conjugated to Horseradish Peroxidase (HRP) is added to each microplate well and incubated. Then a TMB substrate solution is added to each well. Only those wells that contain Collagen alpha-1(III) chain, biotin-conjugated antibody and enzyme-conjugated Avidin will exhibit a change in color. The enzyme-substrate reaction is terminated by the addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm +/- 2 nm. The concentration of Collagen alpha-1(III) chain in the samples is then determined by comparing the O.D. of the samples to the standard curve.

111,907 Da

collagen type III alpha 1

collagen alpha-1(III) chain

Collagen alpha-1(III) chain

CO3A1_HUMAN

This gene encodes the pro-alpha1 chains of type III collagen, a fibrillar collagen that is found in extensible connective tissues such as skin, lung, uterus, intestine and the vascular system, frequently in association with type I collagen. Mutations in this gene are associated with Ehlers-Danlos syndrome types IV, and with aortic and arterial aneurysms. Two transcripts, resulting from the use of alternate polyadenylation signals, have been identified for this gene. [provided by R. Dalgleish, Feb 2008]

CO3A1: Collagen type III occurs in most soft connective tissues along with type I collagen. Defects in COL3A1 are a cause of Ehlers-Danlos syndrome type 3 (EDS3); also known as benign hypermobility syndrome. EDS is a connective tissue disorder characterized by hyperextensible skin, atrophic cutaneous scars due to tissue fragility and joint hyperlaxity. EDS3 is a form of Ehlers-Danlos syndrome characterized by marked joint hyperextensibility without skeletal deformity. Defects in COL3A1 are the cause of Ehlers-Danlos syndrome type 4 (EDS4). EDS is a connective tissue disorder characterized by hyperextensible skin, atrophic cutaneous scars due to tissue fragility and joint hyperlaxity. EDS4 is the most severe form of the disease. It is characterized by the joint and dermal manifestations as in other forms of the syndrome, characteristic facial features (acrogeria) in most patients, and by proneness to spontaneous rupture of bowel and large arteries. The vascular complications may affect all anatomical areas. Defects in COL3A1 are a cause of susceptibility to aortic aneurysm abdominal (AAA). AAA is a common multifactorial disorder characterized by permanent dilation of the abdominal aorta, usually due to degenerative changes in the aortic wall. Histologically, AAA is characterized by signs of chronic inflammation, destructive remodeling of the extracellular matrix, and depletion of vascular smooth muscle cells. Belongs to the fibrillar collagen family. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: Secreted; Secreted, signal peptide; Motility/polarity/chemotaxis; Cell adhesion; Extracellular matrix

Chromosomal Location of Human Ortholog: 2q31

Cellular Component: collagen type III; endoplasmic reticulum lumen; extracellular matrix; extracellular region; extracellular space

Molecular Function: extracellular matrix structural constituent; integrin binding; metal ion binding; platelet-derived growth factor binding; protein binding; SMAD binding

Biological Process: aging; axon guidance; cell-matrix adhesion; cerebral cortex development; collagen catabolic process; collagen fibril organization; extracellular matrix disassembly; extracellular matrix organization and biogenesis; fibril organization and biogenesis; gut development; heart development; integrin-mediated signaling pathway; negative regulation of immune response; peptide cross-linking; platelet activation; positive regulation of Rho protein signal transduction; receptor-mediated endocytosis; regulation of immune response; response to cytokine stimulus; response to mechanical stimulus; response to radiation; skeletal development; skin development; transforming growth factor beta receptor signaling pathway; wound healing

Disease: Ehlers-danlos Syndrome, Type Iii; Ehlers-danlos Syndrome, Type Iv, Autosomal Dominant

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