ELISA/assay

Mouse Collagen Type III ELISA Kit

MBS720538

48-Strip-Wells

470 USD

ELISA Kit

Mouse Collagen Type III ELISA Kit

Collagen Type III

Mouse Collagen Type III (Col III) ELISA Kit; Mouse Collagen Type III ELISA Kit; Collagen Type III; Collagen Type III (Mouse)

collagen type III alpha 1

Col III

Mouse

This assay has high sensitivity and excellent specificity for detection of CoL-3. No significant cross-reactivity or interference between CoL-3 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between CoL-3 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 ng/mL.

Mouse ELISA Kit

Intended Uses This CoL-3 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Mouse CoL-3. This ELISA kit for research use only, not for therapeutic or diagnostic applications!. Principle of the Assay: CoL-3 ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-CoL-3 antibody and an CoL-3-HRP conjugate. The assaysample and buffer are incubated together with CoL-3-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-3 concentration since CoL-3 from samples and CoL-3-HRP conjugate compete for the anti-CoL-3 antibody binding site. Since the number of sites is limited, as more sites are occupied by CoL-3 from the sample, fewer sites are left to bind CoL-3-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The CoL-3 concentration in each sample is interpolated from this standard curve.

494319369

AGL34959

Focal Adhesion Pathway (83067); Focal Adhesion Pathway (478); MAPK Signaling Pathway (83048); MAPK Signaling Pathway (456); Salmonella Infection Pathway (375172); Salmonella Infection Pathway (375149)

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: Cell adhesion; Secreted, signal peptide; Secreted; Motility/polarity/chemotaxis; Extracellular matrix. 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; extracellular matrix structural constituent; metal ion binding; platelet-derived growth factor binding; SMAD binding. Biological Process: integrin-mediated signaling pathway; skin development; axon guidance; receptor-mediated endocytosis; platelet activation; 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; extracellular matrix disassembly; collagen catabolic process; response to radiation; gut development; response to mechanical stimulus; response to cytokine stimulus; transforming growth factor beta receptor signaling pathway; fibril organization and biogenesis; peptide cross-linking; cerebral cortex development; 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