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The following MAPmates™ should not be plexed together:
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48-602MAG
Buffer Detection Kit for Magnetic Beads
1 Kit
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Aggrecan (CSPG1, CSPCP, or CSPGCP) is a chondroitin-sulfate proteoglycan belonging to the family of letican proteins. Aggrecan is a large globar structure containing multiple domains including carbohydrate-recognition domains; complement binding protein domains; immunoglobulin domains; proteoglycan tandem repeats; and in some cases, EGF-like domains. It can be degraded by aggrecanase. The N-terminus of aggrecan binds ECM hyaluronan in the presence of the linking protein, and forms complex aggregates, whereas the C-terminus binds a number of other ECM proteins including tenascins, glycolipids, and fibulins. Aggrecan is a major component of cartilage tissue and it enables this tissue to withstand compression by maintaining the viso-elastic properties of cartilage. Aggrecan may also facilitate neural maturation and plasticity by contributing to the formation of perineuronal nets in the developing CNS.
References
Product Information
Format
Purified
Control
A1D1 purified protein from bovine tissue lysate
Presentation
Purified mouse monoclonal IgG1κ in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.
Anti-Aggrecan Antibody, clone 6B4 is an antibody against Aggrecan for use in Western Blotting & IHC.
Key Applications
Western Blotting
Immunohistochemistry
Application Notes
Immunofluorescent Analysis: A representative lot was used by an independent laboratory in human femoral chondrocytes (Williams, R., et al. (2010). PLoS One. 5(10):e13246.).
Immunohistochemistry Analysis: A representative lot was used by an independent laboratory in human chartilage tissue (Williams, R., et al. (2010). PLoS One. 5(10):e13246.).
Biological Information
Immunogen
Ovalbumin-conjugated linear peptide corresponding to human Aggrecan.
Clone
6B4
Concentration
Please refer to the Certificate of Analysis for the lot-specific concentration.
Host
Mouse
Isotype
IgG1κ
Species Reactivity
Bovine
Human
Species Reactivity Note
Demonstrated to react with Bovine. Predicted to react with Human based on 100% sequence homology.
This gene is a member of the aggrecan/versican proteoglycan family. The encoded protein is an integral part of the extracellular matrix in cartilagenous tissue and it withstands compression in cartilage. Mutations in this gene may be involved in skeletal dysplasia and spinal degeneration. Multiple alternatively spliced transcript variants that encode different protein isoforms have been observed in this gene.
FUNCTION: This proteoglycan is a major component of extracellular matrix of cartilagenous tissues. A major function of this protein is to resist compression in cartilage. It binds avidly to hyaluronic acid via an N-terminal globular region.
SUBUNIT STRUCTURE: Interacts with FBLN1. Interacts with COMP.
TISSUE SPECIFICITY: Restricted to cartilages.
DEVELOPMENTAL STAGE: Expression was detected in chondrocytes throughout the developing skeleton.
DOMAIN: Two globular domains, G1 and G2, comprise the N-terminus of the proteoglycan, while another globular region, G3, makes up the C-terminus. G1 contains Link domains and thus consists of three disulfide-bonded loop structures designated as the A, B, B' motifs. G2 is similar to G1. The keratan sulfate (KS) and the chondroitin sulfate (CS) attachment domains lie between G2 and G3.
POST-TRANSLATIONAL MODIFICATION: Contains mostly chondroitin sulfate, but also keratan sulfate chains, N-linked and O-linked oligosaccharides. The release of aggrecan fragments from articular cartilage into the synovial fluid at all stages of human osteoarthritis is the result of cleavage by aggrecanase.
INVOLVEMENT IN DISEASE: Defects in ACAN are the cause of spondyloepiphyseal dysplasia type Kimberley (SEDK). Spondyloepiphyseal dysplasias are a heterogeneous group of congenital chondrodysplasias that specifically affect epiphyses and vertebrae. The autosomal dominant SEDK is associated with premature degenerative arthropathy. Defects in ACAN are the cause of spondyloepimetaphyseal dysplasia aggrecan type (SEMD-ACAN). A bone disease characterized by severe short stature, macrocephaly, severe midface hypoplasia, short neck, barrel chest and brachydactyly. The radiological findings comprise long bones with generalized irregular epiphyses with widened metaphyses, especially at the knees, platyspondyly, and multiple cervical-vertebral clefts. Defects in ACAN are the cause of osteochondritis dissecans short stature and early-onset osteoarthritis (OD) [MIM:165800]. It is a type of osteochondritis defined as a separation of cartilage and subchondral bone from the surrounding tissue, primarily affecting the knee, ankle and elbow joints. It is clinically characterized by multiple osteochondritic lesions in knees and/or hips and/or elbows, disproportionate short stature and early-onset osteoarthritis.
~60 kDa observed. Uniprot describes three isoforms at ~250 kDa, ~246 kDa, and ~239 kDa. Aggrecan is degraded by aggrecanase into a ~60 kDa protein and other higher molecular weight products (Lemons, M. L. et al. (2001). J Neurosci. 21(13):4772-4781. Forsang, A. J. et al. (1995). Biochem J. 310(Pt 1):337-343.).
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Safety Information according to GHS
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Product Usage Statements
Quality Assurance
Evaluated by Western Blot in A1D1 purified protein from bovine tissue lysate.
Western Blot Analysis: 1 µg/mL of this antibody detected Aggrecan in 10 µg of purified protein from bovine tissue lysate.
Usage Statement
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Identification and clonal characterisation of a progenitor cell sub-population in normal human articular cartilage. Williams, Rebecca, et al. PLoS ONE, 5: e13246 (2010)
2010
Articular cartilage displays a poor repair capacity. The aim of cell-based therapies for cartilage defects is to repair damaged joint surfaces with a functional replacement tissue. Currently, chondrocytes removed from a healthy region of the cartilage are used but they are unable to retain their phenotype in expanded culture. The resulting repair tissue is fibrocartilaginous rather than hyaline, potentially compromising long-term repair. Mesenchymal stem cells, particularly bone marrow stromal cells (BMSC), are of interest for cartilage repair due to their inherent replicative potential. However, chondrocyte differentiated BMSCs display an endochondral phenotype, that is, can terminally differentiate and form a calcified matrix, leading to failure in long-term defect repair. Here, we investigate the isolation and characterisation of a human cartilage progenitor population that is resident within permanent adult articular cartilage.
Chondrocytes are the only cells found in healthy cartilage. They produce and maintain the cartilaginous matrix, which consists mainly of collagen and proteoglycans. Learn More >>
