SpecificitySpecificity was ascertained by competition ELISA. Complete inhibition is found if the antibody was preincubated with collagen type III. Inhibition by other types of collagens was observed only at 20-50 times higher concentration. No inhibition was found with fibronectin, fibrinogen and laminin. Characteristic immunostaining pictures of frozen sections of human kidney, liver, skin and heart are produced to certify batch quality.
Extensively purified native collagen type III extracted from human skin.
Human kidney, liver, skin and heart for IHC-Fr.
Storage instructionsShipped at 4°C. Store at +4°C.
Storage bufferThe antibody was extracted into dilute acidic buffer after mild pepsin digestion.
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Purification notesPooled antisera are passed over DEAE cellulose to produce IgG enriched fraction, which is further subjected to absorption with immobilized total human serum proteins in order to remove non specific antibodies. Next, the antisera fraction is absorbed with immunobilized collagen types I, II, IV and V to remove cross reactive antibodies to antigenic determinants common for various collagen types. The affinity purified antibody ab24129 is obtained by binding to immobilized native human collagen type III (the antigen used for immunization), followed by elution with acidic buffer, neutralisation, dialysis, dispensing and lyophilization.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Application notesDot: Use at an assay dependent dilution.
ELISA: Use at an assay dependent dilution.
IHC-Fr: Antibodies can be diluted at least 1/20 for immunohistochemical procedures if Peroxidase labeled secondary antibodies are applied. If a FITC labeled secondary antibody is used the antibody can be diluted 1/10.
Also recommended for use in immunostaining of cultered human cells.
Not tested in other applications.
Optimal dilutions/concentrations should be determined by the end user.
FunctionCollagen type III occurs in most soft connective tissues along with type I collagen.
Involvement in diseaseDefects 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 the cause of Ehlers-Danlos syndrome type 4 (EDS4) [MIM:130050]. 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) [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.
Sequence similaritiesBelongs to the fibrillar collagen family. Contains 1 fibrillar collagen NC1 domain. Contains 1 VWFC domain.
Post-translational modificationsProline residues at the third position of the tripeptide repeating unit (G-X-Y) are hydroxylated in some or all of the chains. O-linked glycan consists of a Glc-Gal disaccharide bound to the oxygen atom of a post-translationally added hydroxyl group.
Cellular localizationSecreted > extracellular space > extracellular matrix.