MAB5210
Anti-Phosphacan Antibody, clone 122.2
ascites fluid, clone 122.2, Chemicon®
别名:
Receptor Tyrosine Phosphatase beta
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关于此项目
UNSPSC Code:
12352203
NACRES:
NA.41
eCl@ss:
32160702
Conjugate:
unconjugated
Clone:
122.2, monoclonal
Application:
ICC, IHC, WB
Citations:
7
biological source
mouse
conjugate
unconjugated
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.
Application
Anti-Phosphacan Antibody, clone 122.2 detects level of Phosphacan & has been published & validated for use in WB, IC, IH.
Research Category
Neuroscience
Neuroscience
Research Sub Category
Growth Cones & Axon Guidance
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.
Immunocytochemistry: 1:10
Immunohistochemistry on 4% paraformaldehyde fixed tissue: 1:1,000
Immunoprecipitation
Optimal working dilutions must be determined by the end user.
Biochem/physiol Actions
Phosphacan (Receptor Tyrosine Phosphatase Beta). Recognizes the core protein.
Physical form
Ascites fluid. Liquid. Contains no preservative.
Preparation Note
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.
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.
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存储类别
10 - Combustible liquids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
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
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
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
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
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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