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Key Documents

MAB5204

Sigma-Aldrich

Anti-Agrin Antibody

Chemicon®, from mouse

Synonyme(s) :

Anti-AGRIN, Anti-CMSPPD

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About This Item

Code UNSPSC :
12352203
eCl@ss :
32160702
Nomenclature NACRES :
NA.41

Source biologique

mouse

Niveau de qualité

Forme d'anticorps

purified immunoglobulin

Type de produit anticorps

primary antibodies

Clone

monoclonal

Espèces réactives

mouse, rat

Fabricant/nom de marque

Chemicon®

Technique(s)

immunocytochemistry: suitable
western blot: suitable

Isotype

IgG1

Numéro d'accès NCBI

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... AGRN(375790)

Spécificité

MAB5204 recognizes rat and mouse agrin. The epitope has been mapped near the splicing site Z. Binding of this antibody to agrin causes marked reduction in nAChR clusters.

Immunogène

Recombinant rat agrin (C-terminal construct)

Application

Anti-Agrin Antibody is an antibody against Agrin for use in WB & IC.
Immunocytochemistry: 10 μg/mL

Optimal working dilutions must be determined by the end user.
Research Category
Neuroscience
Research Sub Category
Growth Cones & Axon Guidance

Synapse & Synaptic Biology

Forme physique

Format: Purified
Purified immunoglobulin. Liquid in PBS containing 50% glycerol and 0.09% sodium azide.

Stockage et stabilité

Maintain lyophilized at material -20°C or below for up to 12 months. After reconstitution maintain at -20°C to -70°C in undiluted aliquots for up to 6 months. Avoid repeated freeze/thaw cycles.

Autres remarques

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Informations légales

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

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 2


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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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.

Consulter la Bibliothèque de documents

The COOH-terminal domain of agrin signals via a synaptic receptor in central nervous system neurons.
Hoover, CL; Hilgenberg, LG; Smith, MA
The Journal of cell biology null
Nandor Nagy et al.
Development (Cambridge, England), 145(9) (2018-04-22)
The enteric nervous system (ENS) arises from neural crest cells that migrate, proliferate, and differentiate into enteric neurons and glia within the intestinal wall. Many extracellular matrix (ECM) components are present in the embryonic gut, but their role in regulating
Silvia Scaricamazza et al.
British journal of pharmacology, 179(8), 1732-1752 (2021-11-17)
Amyotrophic lateral sclerosis (ALS), a neurodegenerative disease characterized by the degeneration of upper and lower motor neurons, progressive wasting and paralysis of voluntary muscles and is currently incurable. Although considered to be a pure motor neuron disease, increasing evidence indicates
Zhenxi Zhang et al.
Proceedings of the National Academy of Sciences of the United States of America, 110(48), 19348-19353 (2013-11-06)
The motor neuron (MN) degenerative disease, spinal muscular atrophy (SMA) is caused by deficiency of SMN (survival motor neuron), a ubiquitous and indispensable protein essential for biogenesis of snRNPs, key components of pre-mRNA processing. However, SMA's hallmark MN pathology, including
Jessica L Mueller et al.
Stem cells translational medicine, 13(5), 490-504 (2024-02-22)
Regenerative cell therapy to replenish the missing neurons and glia in the aganglionic segment of Hirschsprung disease represents a promising treatment option. However, the success of cell therapies for this condition are hindered by poor migration of the transplanted cells.

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