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Merck

P8874

Sigma-Aldrich

Monoclonal Anti-Phosphocan in Maus hergestellte Antikörper

~2 mg/mL, clone 122.2, purified immunoglobulin, buffered aqueous solution

Synonym(e):

Anti-PTPRB, Anti-Receptor-type Protein-tyrosine phosphatase β

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About This Item

MDL-Nummer:
UNSPSC-Code:
12352203
NACRES:
NA.41

Biologische Quelle

mouse

Qualitätsniveau

Konjugat

unconjugated

Antikörperform

purified immunoglobulin

Antikörper-Produkttyp

primary antibodies

Klon

122.2, monoclonal

Form

buffered aqueous solution

Mol-Gew.

antigen ~180 kDa (higher band may be present)

Speziesreaktivität

rat

Verpackung

antibody small pack of 25 μL

Konzentration

~2 mg/mL

Methode(n)

immunocytochemistry: suitable
immunohistochemistry: suitable
western blot: 0.2-0.4 μg/mL using total extract of rat brain

Isotyp

IgM

UniProt-Hinterlegungsnummer

Versandbedingung

dry ice

Lagertemp.

−20°C

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

Allgemeine Beschreibung

Monoclonal Anti-Phosphacan (mouse IgM isotype) is derived from the hybridoma 122.2 produced by the fusion of mouse myeloma cells (P3X cells) and splenocytes from BALB/c mice immunized with rat brain proteoglycans. Chondroitin sulfate proteoglycans are neural cell adhesion molecules (NCAM) ligands present in the brain extracellular matrix (ECM). Phosphacan protein is expressed mainly in astrocytes and is a ligand for NCAM. Phosphacan is the soluble extracellular domain of the receptor-type transmembrane protein tyrosine phosphatase (RPTPb).

Immunogen

rat brain proteoglycans.

Anwendung

Monoclonal Anti-Phosphacan antibody produced in mouse has been used in:
  • immunoblotting
  • immunohistochemistry
  • immunocytochemistry.

Biochem./physiol. Wirkung

Phosphacan levels elevates during late embryogenesis. It reaches a plateau two weeks postnatal before reaching stable. Receptor-type transmembrane protein tyrosine phosphatase (RPTPb) functions to promote primary tecal neurons neurite growth, neural migration and also induces cell adhesion. Both phosphacan and RPTPb can bind to NCAM and tenascin-C and −R. Phosphacan can oppose RPTPb by competing for its binding sites. Both in hippocampal and spinal cord neurons, phosphacan can affect neuronal adhesion and neurite outgrowth.

Physikalische Form

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.

Haftungsausschluss

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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Lagerklassenschlüssel

10 - Combustible liquids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable

Persönliche Schutzausrüstung

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)


Analysenzertifikate (COA)

Suchen Sie nach Analysenzertifikate (COA), indem Sie die Lot-/Chargennummer des Produkts eingeben. Lot- und Chargennummern sind auf dem Produktetikett hinter den Wörtern ‘Lot’ oder ‘Batch’ (Lot oder Charge) zu finden.

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In der Dokumentenbibliothek finden Sie die Dokumentation zu den Produkten, die Sie kürzlich erworben haben.

Die Dokumentenbibliothek aufrufen

Receptor protein tyrosine phosphatases in nervous system development
Johnson KG and Van Vactor D
Physiological Reviews, 83(1), 1-24 (2003)
The tissue plasminogen activator (tPA/Plasmin) extracellular proteolytic system regulates seizure-induced hippocampal mossy fiber outgrowth through a proteoglycan substrate
Wu YP, et al.
The Journal of cell biology, 148(6), 1295-1304 (2000)
Y P Wu et al.
The Journal of cell biology, 148(6), 1295-1304 (2000-03-22)
Short seizure episodes are associated with remodeling of neuronal connections. One region where such reorganization occurs is the hippocampus, and in particular, the mossy fiber pathway. Using genetic and pharmacological approaches, we show here a critical role in vivo for
RGMa mediates reactive astrogliosis and glial scar formation through TGFbeta1/Smad2/3 signaling after stroke
Zhang R, et al.
Cell Death and Differentiation, 25(8), 1503-1503 (2018)
Rongrong Zhang et al.
Cell death and differentiation, 25(8), 1503-1516 (2018-02-06)
In response to stroke, astrocytes become reactive astrogliosis and are a major component of a glial scar. This results in the formation of both a physical and chemical (production of chondroitin sulfate proteoglycans) barrier, which prevent neurite regeneration that, in

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