ELISA/assay

Rat Collagen Type III ELISA Kit

MBS721887

48-Strip-Wells

470 USD

ELISA Kit

Rat Collagen Type III ELISA Kit

Collagen Type III

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

collagen type III alpha 1

Col III

Rat

This assay has high sensitivity and excellent specificity for detection of CoL3. No significant cross-reactivity or interference between CoL3 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between CoL3 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: Sandwich. Sensitivity: 1.0 ng/mL.

Rat ELISA Kit

For samples: Serum, plasma, cell culture supernatants, body fluid and tissue homogenate . INTENDED USE This CoL3 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Rat CoL3. This ELISA kit for research use only, not for therapeutic or diagnostic applications! . PRINCIPLE OF THE ASSAY CoL3 ELISA kit applies the quantitative sandwich enzyme immunoassay technique. The microtiter plate has been pre-coated with a monoclonal antibody specific for CoL3. Standards or samples are then added to the microtiter plate wells and CoL3 if present, will bind to the antibody pre-coated wells. In order to quantitatively determine the amount of CoL3 present in the sample, a standardized preparation of horseradish peroxidase (HRP)-conjugated polyclonal antibody, specific for CoL3 are added to each well to “sandwich” the CoL3 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 CoL3 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 CoL3 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: Secreted, signal peptide; Motility/polarity/chemotaxis; 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; extracellular matrix structural constituent; platelet-derived growth factor binding; SMAD binding. Biological Process: skin development; integrin-mediated signaling pathway; platelet activation; receptor-mediated endocytosis; axon guidance; extracellular matrix organization and biogenesis; collagen fibril organization; wound healing; cell-matrix adhesion; heart development; 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; transforming growth factor beta receptor signaling pathway; response to cytokine stimulus; 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