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
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
mouse
Quality Level
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
Gene Information
rat ... Cspg4(81651)
Related Categories
Specificity
Chondroitin sulfate proteoglycan (CSPG), carbohydrate epitope
Immunogen
Epitope: carbohydrate epitope
Feline brain proteoglycans
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.
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
Cell Structure
Research Sub Category
Integrins
Integrins
Physical form
Liquid with 0.1% sodium azide.
Storage and Stability
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
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
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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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
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
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
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
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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