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MAB2029

Sigma-Aldrich

Anti-Chondroitin Sulfate Proteoglycan Antibody, clone 9.2.27

clone 9.2.27, Chemicon®, from mouse

Synonym(s):

Anti-CSPG4A, Anti-MCSP, Anti-MCSPG, Anti-MEL-CSPG, Anti-MSK16, Anti-NG2

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

mouse

Quality Level

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

9.2.27, monoclonal

species reactivity

human

manufacturer/tradename

Chemicon®

technique(s)

flow cytometry: suitable
immunofluorescence: suitable
immunoprecipitation (IP): suitable

isotype

IgG2a

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... CSPG4(1464)

Specificity

Recognizes mature chondroitin sulfate proteoglycan core glycoprotein of 250 kDa as well as precursor polypeptides of 210, 220 and 240 kDa (Bumoi et al., 1984). Reacts with human melanoma, glioma and proliferating brain endothelial cells.

Immunogen

Human M14 melanoma cell extract depleted of fibronectin and bound by lens culinaris lectin-Sepharose (Morgan et al., 1981).

Application

Detect Chondroitin Sulfate Proteoglycan using this Anti-Chondroitin Sulfate Proteoglycan Antibody, clone 9.2.27 validated for use in FC, IF & IP.
Immunofluorescence microscopy of cells in culture (Bumoi et al., 1984; Schrappe et al., 1992). Also, Legg J et al (2003) Development 130:6049-6063 {3% PFA fixed frozen sections}.

Immunoelectron microscopy (Bumoi et al., 1984)

Immunoprecipitation: 1μg/10E6 cells (Bumoi et al., 1984; Morgan et al., 1981)

FACS analysis: 1-2μg/10E6 cells

Functional block of melanoma cell spreading (Morgan et al., 1981), glioma cell proliferation3 and tumor growth in nude mice (Morgan et al., 1981; Schrappe et al., 1992).

Optimal working dilutions must be determined by end user.
Research Category
Cell Structure
Research Sub Category
ECM Proteins

Physical form

Format: Purified
Purified immunoglobulin in 0.02M PBS pH 7.6, 0.25M NaCl containing 0.1% sodium azide.

Storage and Stability

Maintain between 2 and 8°C in undiluted aliquots for up to 6 months.

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Legal Information

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

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.

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Storage Class Code

10 - Combustible liquids

WGK

WGK 2

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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The microSiM (µSiM) is a membrane-based culture platform for modeling the blood-brain barrier (BBB). Unlike conventional membrane-based platforms, the µSiM provides experimentalists with new capabilities, including live cell imaging, unhindered paracrine signaling between 'blood' and 'brain' chambers, and the ability to
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Sprouting of angiogenic perivascular cells is thought to be highly dependent upon autocrine and paracrine growth factor stimulation. Accordingly, we report that corneal angiogenesis induced by ectopic FGF implantation is strongly impaired in NG2/CSPG4 proteoglycan (PG) null mice known to
Henrietta M Nielsen et al.
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Neuron Glial 2 (NG2) cells are glial cells known to serve as oligodendrocyte progenitors as well as modulators of the neuronal network. Altered NG2 cell morphology and up-regulation as well as increased shedding of the proteoglycan NG2 expressed on the
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The population of brain pericytes, a cell type important for vessel stability and blood brain barrier function, has recently been shown altered in patients with Alzheimer's disease (AD). The underlying reason for this alteration is not fully understood, but progressive

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