Anti-Collagen Type III

Collagen Type III from human and bovine placentaSpecies Reactivity: human bovine Application: Anti-Collagen antibodies have been used for indirect trapping ELISA for quantitation of antigen in serum using a standard curve for immunoprecipitation and for native (non-denaturing non-dissociating) PAGE and western blotting for highly sensitive qualitative analysis. Recommended

User OptimizedPhysical State: Liquid (sterile filtered)Purity and

Lot specific

None We produces highly active antibodies and conjugates to collagens. Collagens are highly conserved throughout evolution and are characterized by an uninterrupted \" Glycine-X-Y\" triplet repeat that is a necessary part of the triple helical structure. For these reasons it is often extremely difficult to generate antibodies with specificities to collagens. The development of type-specific antibodies is dependent on NON-DENATURED three-dimensional epitopes. We extensively purifies collagens for immunization from human and bovine placenta and cartilage by limited pepsin digestion and selective salt precipitation. This preparation results in a native conformation of the protein. Antibodies are isolated from rabbit antiserum and are extensively cross-adsorbed by immunoaffinity purification to produce \' type\' -specific antibodies. Greatly diminished reactivity and selectivity of these antibodies will result if denaturing and reducing conditions are used for SDSPAGE and immunoblotting.

Trimers of identical alpha 1(III) chains. The chains are linked to each other by interchain disulfide bonds. Trimers are also cross-linked via hydroxylysines.

Proline residues at the third position of the tripeptide repeating unit (G-X-Y) are hydroxylated in some or all of the chains.

Defects in COL3A1 are a cause of Ehlers-Danlos syndrome type 3 (EDS3) [MIM:130020]; 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 a cause of susceptibility to aortic aneurysm abdominal (AAA) [MIM:100070]. 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.

Contains 1 VWFC domain.