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Merck

P8874

Sigma-Aldrich

Monoclonal Anti-Phosphacan antibody produced in mouse

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

Synonim(y):

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

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About This Item

Numer MDL:
Kod UNSPSC:
12352203
NACRES:
NA.41

pochodzenie biologiczne

mouse

Poziom jakości

białko sprzężone

unconjugated

forma przeciwciała

purified immunoglobulin

rodzaj przeciwciała

primary antibodies

klon

122.2, monoclonal

Postać

buffered aqueous solution

masa cząsteczkowa

antigen ~180 kDa (higher band may be present)

reaktywność gatunkowa

rat

opakowanie

antibody small pack of 25 μL

stężenie

~2 mg/mL

metody

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

izotyp

IgM

numer dostępu UniProt

Warunki transportu

dry ice

temp. przechowywania

−20°C

docelowa modyfikacja potranslacyjna

unmodified

informacje o genach

Opis ogólny

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.

Zastosowanie

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

Działania biochem./fizjol.

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.

Postać fizyczna

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

Oświadczenie o zrzeczeniu się odpowiedzialności

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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Kod klasy składowania

10 - Combustible liquids

Klasa zagrożenia wodnego (WGK)

WGK 3

Temperatura zapłonu (°F)

Not applicable

Temperatura zapłonu (°C)

Not applicable

Środki ochrony indywidualnej

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


Certyfikaty analizy (CoA)

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Masz już ten produkt?

Dokumenty związane z niedawno zakupionymi produktami zostały zamieszczone w Bibliotece dokumentów.

Odwiedź Bibliotekę dokumentów

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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