Heparan sulfate proteoglycan of basement membrane; HSPG; Hspg2; LG3 peptide; Perlecan; PLC; SJS1

For Research Use Only. Not for use in diagnostic procedures.

Monoclonal

IgG2a, kappa

A7L6

Rat

This MAb specifically precipitates heterogeneous material of high MW, identified as perlecan, a major heparan-sulfate proteoglycan (HSPG) within all basement membranes and cell surfaces. It does not cross-react with laminin, fibronectin, or dermatran sulfate proteoglycan. Because of perlecan s strategic location and ability to store and protect growth factors, it has been strongly implicated in the control of tumor cell growth and metastatic behavior. Perlecan possesses angiogenic and growth-promoting attributes primarily by acting as a co-receptor for basic fibroblast growth factor (FGF-2). Suppression of perlecan causes substantial inhibition of neoplastic growth and neovascularization. Thus, perlecan is a potent inducer of neoplasm growth and angiogenesis in vivo and therapeutic interventions targeting this key modulator of tumor progression may improve neoplastic treatment.

200ug/ml of Ab purified from Bioreactor Concentrate by Protein A/G. Prepared in 10mM PBS with 0.05% BSA & 0.05% azide. Also available WITHOUT BSA at 1.0mg/ml.

Antibody without azide - store at -20 to -80 degree C. Antibody is stable for 24 months. Non-hazardous. No MSDS required.

Small volumes of anti-HSPG2 antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Flow Cytometry (FC/FACS), Immunofluorescence (IF), Immunohistochemistry (IHC) Formalin

Flow Cytometry (0.5-1 ug/million cells in 0.1 ml)
Immunofluorescence (0.5-1.0 ug/ml)
Immunohistology (Formalin-fixed) (1-2ug/ml for 30 minutes at RT)
(Staining of formalin/paraffin tissues Requires boiling tissue sections in 10mM citrate buffer, pH 6.0, for 10-20 min followed by cooling at RT for 20 min.)

Formalin-fixed, paraffin-embedded human Testicular Carcinoma stained with Heparan Sulfate Monoclonal Antibody (A7L6).

>400kDa

heparan sulfate proteoglycan 2

basement membrane-specific heparan sulfate proteoglycan core protein

Basement membrane-specific heparan sulfate proteoglycan core protein

HSPG; PLC??[Similar Products]

PGBM_HUMAN

This gene encodes the perlecan protein, which consists of a core protein to which three long chains of glycosaminoglycans (heparan sulfate or chondroitin sulfate) are attached. The perlecan protein is a large multidomain proteoglycan that binds to and cross-links many extracellular matrix components and cell-surface molecules. It has been shown that this protein interacts with laminin, prolargin, collagen type IV, FGFBP1, FBLN2, FGF7 and transthyretin, etc., and it plays essential roles in multiple biological activities. Perlecan is a key component of the vascular extracellular matrix, where it helps to maintain the endothelial barrier function. It is a potent inhibitor of smooth muscle cell proliferation and is thus thought to help maintain vascular homeostasis. It can also promote growth factor (e.g., FGF2) activity and thus stimulate endothelial growth and re-generation. It is a major component of basement membranes, where it is involved in the stabilization of other molecules as well as being involved with glomerular permeability to macromolecules and cell adhesion. Mutations in this gene cause Schwartz-Jampel syndrome type 1, Silverman-Handmaker type of dyssegmental dysplasia, and tardive dyskinesia. Alternative splicing of this gene results in multiple transcript variants. [provided by RefSeq, May 2014]

HSPG2: Integral component of basement membranes. Component of the glomerular basement membrane (GBM), responsible for the fixed negative electrostatic membrane charge, and which provides a barrier which is both size- and charge-selective. It serves as an attachment substrate for cells. Plays essential roles in vascularization. Critical for normal heart development and for regulating the vascular response to injury. Also required for avascular cartilage development. Defects in HSPG2 are the cause of Schwartz-Jampel syndrome (SJS1); a rare autosomal recessive disorder characterized by permanent myotonia (prolonged failure of muscle relaxation) and skeletal dysplasia, resulting in reduced stature, kyphoscoliosis, bowing of the diaphyses and irregular epiphyses. Defects in HSPG2 are the cause of dyssegmental dysplasia Silverman-Handmaker type (DDSH). The dyssegmental dysplasias are rare, autosomal recessive skeletal dysplasias with anisospondyly and micromelia. There are two recognized types: the severe, lethal DDSH and the milder Rolland-Desbuquois form. Individuals with DDSH also have a flat face, micrognathia, cleft palate and reduced joint mobility, and frequently have an encephalocoele. The endochondral growth plate is short, the calcospherites (which are spherical calcium-phosphorus crystals produced by hypertrophic chondrocytes) are unfused, and there is mucoid degeneration of the resting cartilage.

Protein type: Secreted; Motility/polarity/chemotaxis; Secreted, signal peptide; Cell adhesion

Chromosomal Location of Human Ortholog: 1p36.1-p34

Cellular Component: extracellular matrix; extracellular region; extracellular space; focal adhesion; Golgi lumen; lysosomal lumen; plasma membrane

Molecular Function: protein binding; protein C-terminus binding

Biological Process: cellular protein metabolic process; extracellular matrix disassembly; extracellular matrix organization and biogenesis; glycosaminoglycan biosynthetic process; glycosaminoglycan catabolic process; glycosaminoglycan metabolic process; lipoprotein metabolic process; retinoid metabolic process

Disease: Dyssegmental Dysplasia, Silverman-handmaker Type; Schwartz-jampel Syndrome, Type 1

Folkvord et. al., J Histochem Cytochem, 1989; 37:105-113. Couchman et. al., Matrix, 1989; 9:311-321. Horiguchi et. al., J Histochem Cytochem, 1989; 37:961-970. Ljubimov et. al., Int J Cancer, 1992; 50:562-566. Guelstein et. al., Int J Cancer, 1993; 53:269-277. Ljubimov et. al., Lab Invest, 1995; 72:461-473

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