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P8874

Sigma-Aldrich

Monoclonal Anti-Phosphocan antibody produced in mouse

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

Synonyme(s) :

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

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About This Item

Numéro MDL:
MFCD09265428
Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

mouse

Niveau de qualité

200

Conjugué

unconjugated

Forme d'anticorps

purified immunoglobulin

Type de produit anticorps

primary antibodies

Clone

122.2, monoclonal

Forme

buffered aqueous solution

Poids mol.

antigen ~180 kDa (higher band may be present)

Espèces réactives

rat

Conditionnement

antibody small pack of 25 μL

Concentration

~2 mg/mL

Technique(s)

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

Isotype

IgM

Numéro d'accès UniProt

Q62656

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

rat ... Ptprz1(25613)

Description générale

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).

Immunogène

rat brain proteoglycans.

Application

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

Actions biochimiques/physiologiques

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.

Forme physique

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

Clause de non-responsabilité

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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Code de la classe de stockage

10 - Combustible liquids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Équipement de protection individuelle

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

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Consulter la Bibliothèque de documents

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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