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Merck
CN

MAB1582

Anti-Chondroitin Sulfate Proteoglycan Antibody, carbohydrate epitope, clone Cat-316

ascites fluid, clone Cat-316, Chemicon®

Synonym(s):

CSPG

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About This Item

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

Key Documents

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Product Name

Anti-Chondroitin Sulfate Proteoglycan Antibody, carbohydrate epitope, clone Cat-316, ascites fluid, clone Cat-316, Chemicon®

biological source

mouse

antibody form

ascites fluid

antibody product type

primary antibodies

clone

Cat-316, monoclonal

species reactivity

feline, rat

manufacturer/tradename

Chemicon®

technique(s)

immunocytochemistry: suitable
immunohistochemistry: suitable
immunoprecipitation (IP): suitable
western blot: suitable

isotype

IgM

shipped in

dry ice

target post-translational modification

unmodified

Quality Level

100

Gene Information

rat ... Cspg4(81651)

Application

Anti-Chondroitin Sulfate Proteoglycan Antibody, carbohydrate epitope, clone Cat-316 is an antibody against Chondroitin Sulfate Proteoglycan for use in IP, WB, IC, IH.
Immunohistochemistry: 1:70,000 on 4% paraformaldehyde fixed frozen tissue.

Immunocytochemistry: 1:2,500 on primary cultures of neurons.

Immunoblot: 1:200,000

Immunoprecipitation

Optimal working dilutions must be determined by the end user.
Research Category
Cell Structure
Research Sub Category
Integrins

Biochem/physiol Actions

Chondroitin sulfate proteoglycan (CSPG), carbohydrate epitope

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.

Immunogen

Epitope: carbohydrate epitope
Feline brain proteoglycans

Physical form

Liquid with 0.1% sodium azide.

Preparation Note

Maintain at -20°C in undiluted aliquots for up to 6 months. Avoid repeated freeze/thaw cycles

Legal Information

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

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Storage Class

12 - Non Combustible Liquids

wgk

nwg

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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Shinji Miyata et al.
Frontiers in integrative neuroscience, 12, 3-3 (2018-02-20)
Aggrecan, a chondroitin sulfate (CS) proteoglycan, forms lattice-like extracellular matrix structures called perineuronal nets (PNNs). Neocortical PNNs primarily ensheath parvalbumin-expressing inhibitory neurons (parvalbumin, PV cells) late in brain development. Emerging evidence indicates that PNNs promote the maturation of PV cells
Satomi Nadanaka et al.
Biomolecules, 10(11) (2020-11-05)
The chondroitin sulfate (CS)-rich dense extracellular matrix surrounding neuron cell bodies and proximal dendrites in a mesh-like structure is called a perineuronal net (PNN). CS chains in PNNs control neuronal plasticity by binding to PNN effectors, semaphorin-3A (Sema3A) and orthodenticle
De-Lai Zhao et al.
Molecular medicine reports, 22(4), 2637-2644 (2020-09-19)
Chondrocytes in injured cartilage tissue are susceptible to mechanical loading; mechanical overloading can induce cartilage degeneration. The aim of the present study was to investigate whether mechanical loading can regulate chondrocyte degeneration and angiogenesis via the tissue inhibitor of matrix
Hiroshi Ueno et al.
IBRO reports, 4, 22-37 (2018-08-24)
Specific regions of the cerebral cortex are highly plastic in an organism's lifetime. It is thought that perineuronal nets (PNNs) regulate plasticity, but labeling for Wisteria floribunda agglutinin (WFA), which is widely used to detect PNNs, is observed throughout the
Guixin Zhang et al.
The Journal of comparative neurology, 522(9), 2209-2229 (2013-12-21)
Disability following spinal cord injury is due to failure of axon regeneration, which has been ascribed to environmental factors in the central nervous system and a developmental loss of intrinsic growth capacity in neurons. Recently, the receptor-like protein tyrosine phosphatases

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