Anti-Collagen III antibody (Biotin) (ab24823)

Overview

  • Product nameAnti-Collagen III antibody (Biotin)See all Collagen III primary antibodies ...
  • Description
    Goat polyclonal to Collagen III (Biotin)
  • ConjugationBiotin
  • SpecificityReacts with conformational determinants on human type III collagen as demonstrated by ELISA. May react with type III collagen from other species. Exhibits <10% cross reactivity with collagen type I, II, IV, V and VI. The antibody has not been tested for reactivity with other ECM proteins (e.g., laminin, fibronectin).
  • Tested applicationsDot Blot, ELISA, ICC, IHC-Fr more details
  • Species reactivity
    Reacts with: Human
  • Immunogen

    Human type III collagen.

Properties

Applications

Our Abpromise guarantee covers the use of ab24823 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Notes
Dot Blot Use at an assay dependent dilution.
ELISA 1/1000 - 1/4000.
ICC 1/20 - 1/40.
IHC-Fr 1/20 - 1/40.

Target

  • 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
    modifications
    Proline 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.
  • Target information above from: UniProt accession P02461 The UniProt Consortium
    The Universal Protein Resource (UniProt) in 2010
    Nucleic Acids Res. 38:D142-D148 (2010) .

    Information by UniProt
  • Database links
  • Alternative names
    • CO3A1_HUMAN antibody
    • COL 3A1 antibody
    • COL3A1 antibody
    • Collagen alpha 1(III) chain antibody
    • Collagen alpha-1(III) chain antibody
    • Collagen III alpha 1 chain precursor antibody
    • Collagen III alpha 1 polypeptide antibody
    • Collagen type III alpha 1 (Ehlers Danlos syndrome type IV autosomal dominant) antibody
    • Collagen type III alpha 1 antibody
    • Collagen type III alpha antibody
    • EDS4A antibody
    • Ehlers Danlos syndrome type IV, autosomal dominant antibody
    • Fetal collagen antibody
    • Type III collagen antibody
    see all

References for Anti-Collagen III antibody (Biotin) (ab24823)

ab24823 has not yet been referenced specifically in any publications.

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