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Anti-ADAMTS2 antibody - Carboxyterminal end
See all ADAMTS2 products (6) ...
Rabbit polyclonal to ADAMTS2 - Carboxyterminal end
Ab39197 recognizes the zymogen of ADAMTS2 at 140-130 kD in reduced Western blots, activated forms at 105-94 kD (major bands), and breakdown products at 50 kD and 34 kD in cell culture media and lysates.
Reacts with
Human
Synthetic peptide based on the carboxyterminal end of human ADAMTS2.
(Peptide available as ab41231.)
Liquid
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze / thaw cycles.
Preservative: 0.05% Sodium Azide
Constituents: 50% Glycerol
Concentration information loading...
Immunogen affinity purified
Polyclonal
IgG
Cell Biology >> Proteolysis / Ubiquitin >> Proteolytic enzymes >> Metalloprotease >> ADAM TS
Cancer >> Invasion/microenvironment >> ECM >> Extracellular matrix >> ADAM protein family
Signal Transduction >> Cytoskeleton / ECM >> Extracellular Matrix >> ECM Enzymes >> MMP
Cardiovascular >> Angiogenesis >> Adhesion / ECM >> Matrix Metalloproteinases >> MMP
Our Abpromise guarantee covers the use of ab39197 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
WB: Use at an assay dependent dilution. Predicted molecular weight: 135 kDa. A recommended starting concentration for Western blots is 1:1,000 when using colorimetric substrates such as BCIP/NBT, and 1:5,000 for chemiluminescent substrates. Higher concentrations of antibody may be needed for samples from more distantly related species. EDTA/EGTA treatment of tissues or lysates is required to see latent zymogen. Dilution optimised using Chromogenic detection. Not yet tested in other applications. Optimal dilutions/concentrations should be determined by the end user.
Cleaves the propeptides of type I and II collagen prior to fibril assembly. Does not act on type III collagen. May also play a role in development that is independent of its role in collagen biosynthesis.
Expressed at high level in skin, bone, tendon and aorta and at low levels in thymus and brain.
Defects in ADAMTS2 are the cause of Ehlers-Danlos syndrome type 7C (EDS7C) [MIM:225410]. EDS is a connective tissue disorder characterized by hyperextensible skin, atrophic cutaneous scars due to tissue fragility and joint hyperlaxity. EDS7C is marked by extremely fragile tissues, hyperextensible skin and easy bruising. Facial skin contains numerous folds, as in the cutis laxa syndrome.
Contains 1 disintegrin domain.
Contains 1 peptidase M12B domain.
Contains 1 PLAC domain.
Contains 4 TSP type-1 domains.
The spacer domain and the TSP type-1 domains are important for a tight interaction with the extracellular matrix.
The precursor is cleaved by a furin endopeptidase.
Secreted > extracellular space > extracellular matrix.
Target information above from: UniProt accessionO95450
The UniProt Consortium
The Universal Protein Resource (UniProt) in 2010
Nucleic Acids Res. 38:D142-D148 (2010).
ab39197 has not yet been referenced specifically in any publications.
Publishing research using ab39197? Please let us know so that we can cite the reference in this datasheet
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