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MAB5204

Sigma-Aldrich

Anti-Agrin Antibody

Chemicon®, from mouse

Synonym(e):

Anti-AGRIN, Anti-CMSPPD

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200 μG
CHF 564.00

CHF 564.00


Voraussichtliches Versanddatum16. April 2025


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200 μG
CHF 564.00

About This Item

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

CHF 564.00


Voraussichtliches Versanddatum16. April 2025


Bulk-Bestellung anfordern

Biologische Quelle

mouse

Qualitätsniveau

Antikörperform

purified immunoglobulin

Antikörper-Produkttyp

primary antibodies

Klon

monoclonal

Speziesreaktivität

mouse, rat

Hersteller/Markenname

Chemicon®

Methode(n)

immunocytochemistry: suitable
western blot: suitable

Isotyp

IgG1

NCBI-Hinterlegungsnummer

UniProt-Hinterlegungsnummer

Versandbedingung

dry ice

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

human ... AGRN(375790)

Spezifität

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.

Immunogen

Recombinant rat agrin (C-terminal construct)

Anwendung

Research Category
Neurowissenschaft
Research Sub Category
Wachstumskegel & Axonlenkung

Synapsen & Synapsenbiologie
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.

Physikalische Form

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

Lagerung und Haltbarkeit

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.

Sonstige Hinweise

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

Rechtliche Hinweise

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

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 2


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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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
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.
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
Paul J Thomas et al.
The American journal of pathology, 186(9), 2429-2448 (2016-08-27)
Overexpression of B4GALNT2 (previously GALGT2) inhibits the development of muscle pathology in mouse models of Duchenne muscular dystrophy, congenital muscular dystrophy 1A, and limb girdle muscular dystrophy 2D. In these models, muscle GALGT2 overexpression induces the glycosylation of α dystroglycan
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

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