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MAB5210

Sigma-Aldrich

Anti-Phosphacan Antibody, clone 122.2

ascites fluid, clone 122.2, Chemicon®

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Synonym(s):
Receptor Tyrosine Phosphatase beta
eCl@ss:
32160702
NACRES:
NA.41

biological source

mouse

Quality Level

antibody form

ascites fluid

antibody product type

primary antibodies

clone

122.2, monoclonal

species reactivity

rat

manufacturer/tradename

Chemicon®

technique(s)

immunocytochemistry: suitable
immunohistochemistry: suitable
western blot: suitable

isotype

IgM

UniProt accession no.

shipped in

dry ice

target post-translational modification

unmodified

Gene Information

human ... PTPRZ1(5803)

General description

Phosphacan is a soluble nervous tissue-specific proteoglycan that is thought to regulate axonal outgrowth. It is synthesized by glia and binds to neurons and to the neural cell adhesion molecules tenascin, N-CAM or NG-CAM but not to laminin and fibronectin. Phosphacan acts as a potent inhibitor of cell adhesion and neurite outgrowth.

Specificity

Phosphacan (Receptor Tyrosine Phosphatase Beta). Recognizes the core protein.

Application

Anti-Phosphacan Antibody, clone 122.2 detects level of Phosphacan & has been published & validated for use in WB, IC, IH.
Research Category
Neuroscience
Research Sub Category
Growth Cones & Axon Guidance
Western blot. Recognizes bands at 250, 190, and 180 kDa on western blots of embryonic rat brain extracts.

Immunocytochemistry: 1:10

Immunohistochemistry on 4% paraformaldehyde fixed tissue: 1:1,000

Immunoprecipitation

Optimal working dilutions must be determined by the end user.

Physical form

Ascites fluid. Liquid. Contains no preservative.

Storage and Stability

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

Analysis Note

Control
POSITIVE CONTROL:

embryonic or early post-natal rat brain.

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.

Storage Class

10 - Combustible liquids

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


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Bala T S Susarla et al.
Journal of neurochemistry, 119(4), 868-878 (2011-09-08)
Traumatic injury to the CNS results in increased expression and deposition of chondroitin sulfate proteoglycans (CSPGs) that are inhibitory to axonal regeneration. Transforming growth factor-β (TGF-β) has been implicated as a major mediator of these changes, but the mechanisms through
Frauke Seehusen et al.
PloS one, 11(7), e0159752-e0159752 (2016-07-22)
In demyelinating diseases, changes in the quality and quantity of the extracellular matrix (ECM) may contribute to demyelination and failure of myelin repair and axonal sprouting, especially in chronic lesions. To characterize changes in the ECM in canine distemper demyelinating
Wu-Fu Chen et al.
CNS neuroscience & therapeutics, 21(9), 698-707 (2015-07-21)
To date, no reliable methods have proven effective for treating spinal cord injury (SCI). Even systemic administration of methylprednisolone (MP) remains controversial. We previously reported that intrathecal (i.t.) administration of granulocyte colony-stimulating factor (G-CSF) improves outcome after experimental spinal cord
José Javier Miguel-Hidalgo et al.
Scientific reports, 13(1), 16419-16419 (2023-09-30)
Major depressive disorder (MDD) and chronic unpredictable stress (CUS) in animals feature comparable cellular and molecular disturbances that involve neurons and glial cells in gray and white matter (WM) in prefrontal brain areas. These same areas demonstrate disturbed connectivity with
Verena Haist et al.
Brain pathology (Zurich, Switzerland), 22(2), 188-204 (2011-07-20)
The accumulation of extracellular matrix (ECM) and glial scar formation are considered important factors for the failure of regeneration in central nervous system (CNS) injury and multiple sclerosis. Theiler's murine encephalomyelitis (TME) as a model of multiple sclerosis served to

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