ELISA/assay

Mouse Collagen Type III Alpha 1 ELISA Kit

MBS725166

48-Strip-Wells

470 USD

ELISA Kit

Mouse Collagen Type III Alpha 1 ELISA Kit

Collagen Type III Alpha 1

collagen, type III, alpha 1 (Ehlers-Danlos syndrome type IV, autosomal dominant), isoform CRA_b; Collagen alpha-1(III) chain; collagen alpha-1(III) chain; collagen alpha-1(III) chain; collagen, fetal; alpha1 (III) collagen; Ehlers-Danlos syndrome type IV, autosomal dominant; collagen, type III, alpha 1

COL3a1

COL3A1; COL3A1; EDS4A

CO3A1_HUMAN

Mouse

This assay has high sensitivity and excellent specificity for detection of CoL-3A1. No significant cross-reactivity or interference between CoL-3A1 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between CoL-3A1 and all the analogues, therefore, cross reaction may still exist in some cases.

Store all reagents at 2-8 degree C.

Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate. Assay Type: Competitive. Sensitivity: 1.0 pg/mL.

Intended Uses: This CoL-3A1 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Mouse CoL-3A1. This ELISA kit for research use only, not for therapeutic or diagnostic applications!

Cell Biology

Principle of the assay: CoL-3A1 ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-CoL-3A1 antibody and an CoL-3A1-HRP conjugate. The assay sample and buffer are incubated together with CoL-3A1-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 CoL-3A1 concentration since CoL-3A1 from samples and CoL-3A1-HRP conjugate compete for the anti-CoL-3A1 antibody binding site. Since the number of sites is limited, as more sites are occupied by CoL-3A1 from the sample, fewer sites are left to bind CoL-3A1-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The CoL-3A1 concentration in each sample is interpolated from this standard curve.

119631316

EAX10911.1

111,907 Da

Amoebiasis Pathway (167324); Amoebiasis Pathway (167191); Assembly Of Collagen Fibrils And Other Multimeric Structures Pathway (730306); Binding And Uptake Of Ligands By Scavenger Receptors Pathway (771599); Collagen Biosynthesis And Modifying Enzymes Pathway (645289); Collagen Formation Pathway (645288); ECM-receptor Interaction Pathway (83068); ECM-receptor Interaction Pathway (479); Endothelins Pathway (137958); Extracellular Matrix Organization Pathway (576262)

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: Motility/polarity/chemotaxis; Secreted, signal peptide; Secreted; Extracellular matrix; Cell adhesion. Chromosomal Location of Human Ortholog: 2q31. Cellular Component: extracellular matrix; extracellular space; endoplasmic reticulum lumen; extracellular region; collagen type III. Molecular Function: integrin binding; protein binding; metal ion binding; platelet-derived growth factor binding; extracellular matrix structural constituent; SMAD binding. Biological Process: integrin-mediated signaling pathway; skin development; platelet activation; axon guidance; receptor-mediated endocytosis; extracellular matrix organization and biogenesis; collagen fibril organization; wound healing; heart development; cell-matrix adhesion; negative regulation of immune response; positive regulation of Rho protein signal transduction; collagen catabolic process; extracellular matrix disassembly; response to radiation; gut development; response to mechanical stimulus; response to cytokine stimulus; transforming growth factor beta receptor signaling pathway; fibril organization and biogenesis; cerebral cortex development; peptide cross-linking; skeletal development; aging. Disease: Ehlers-danlos Syndrome, Type Iv, Autosomal Dominant; Ehlers-danlos Syndrome, Type Iii

48-Strip-Wells

470 USD

96-Strip-Wells

675