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Key Documents

AB5664P

Sigma-Aldrich

Anti-Neurite Outgrowth Inhibitor A Antibody

Chemicon®, from rabbit

Synonim(y):

Nogo-A

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About This Item

Kod UNSPSC:
12352203
eCl@ss:
32160702
NACRES:
NA.41

pochodzenie biologiczne

rabbit

Poziom jakości

forma przeciwciała

affinity purified immunoglobulin

rodzaj przeciwciała

primary antibodies

klon

polyclonal

oczyszczone przez

affinity chromatography

reaktywność gatunkowa

human, rat, mouse

producent / nazwa handlowa

Chemicon®

metody

ELISA: suitable
western blot: suitable

numer dostępu UniProt

Warunki transportu

dry ice

docelowa modyfikacja potranslacyjna

unmodified

informacje o genach

human ... RTN4(57142)

Specyficzność

Recognizes rat Neurite Outgrowth Inhibitor Protein A (Nogo-A). The immunogen shows no significant sequence homology with the alternatively spliced shorter forms Nogo-B or Nogo-C.

Immunogen

An 18 amino acid peptide sequence in the middle region of the putative extracellular domain of rat Nogo-A (Chen et al. 2000; GrandPre et al. 2000; Goldberg & Barres 2000; Prinijha et al. 2000; Tessier-Lavigne & Goodman 2000; Nagase et al. 1998).

The immunogen peptide is highly conserved in mouse (94%) and human (83%) Nogo-A.

Zastosowanie

Anti-Neurite Outgrowth Inhibitor A Antibody is an antibody against Neurite Outgrowth Inhibitor A for use in ELISA & WB.
Research Category
Neuroscience
Research Sub Category
Neurochemistry & Neurotrophins

Growth Cones & Axon Guidance
Western blot: 1-10 μg/mL using ECL. The calculated molecular weight of Nogo-A is approximately 135 kDa. However a molecular weight of approximately 180 kDa has been reported for full length Nogo-A (Chen et al. 2000; GrandPre et al. 2000; Goldberg & Barres 2000; Prinijha et al. 2000; Tessier-Lavigne & Goodman 2000; Nagase et al. 1998).

ELISA: 1:10,000-1:100,000 using 50-100 ng control peptide (Catalog Number AG348) per well.

Optimal working dilutions must be determined by the end user.

Powiązanie

Replaces: AB5888

Postać fizyczna

Affinity purified immunoglobulin. Liquid in PBS containing 0.1% BSA.

Przechowywanie i stabilność

Maintain at -20°C in undiluted aliquots for up to 6 months afet date of receipt. Avoid repeated freeze/thaw cycles.

Inne uwagi

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

Informacje prawne

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

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

12 - Non Combustible Liquids

Klasa zagrożenia wodnego (WGK)

WGK 2

Temperatura zapłonu (°F)

Not applicable

Temperatura zapłonu (°C)

Not applicable


Certyfikaty analizy (CoA)

Poszukaj Certyfikaty analizy (CoA), wpisując numer partii/serii produktów. Numery serii i partii można znaleźć na etykiecie produktu po słowach „seria” lub „partia”.

Masz już ten produkt?

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

Odwiedź Bibliotekę dokumentów

Jian-Qiang Lu et al.
Journal of neuropathology and experimental neurology, 72(12), 1135-1144 (2013-11-15)
Activation of signal transducer and activator of transcription 3 (STAT3) by phosphorylation is thought to mediate anti-inflammatory responses to CNS injury. Several studies have reported an increase in phosphorylated STAT3 (pSTAT3) in peripheral T cells and monocytes from patients with
Hong Zhao et al.
Molecular medicine reports, 24(6) (2021-10-14)
Axon regeneration after lesions to the central nervous system (CNS) is largely limited by the presence of growth inhibitory molecules expressed in myelin. Nogo‑A is a principal inhibitor of neurite outgrowth, and blocking the activity of Nogo‑A can induce axonal
Manuela Cerina et al.
Brain structure & function, 223(7), 3091-3106 (2018-05-11)
Alterations in cortical cellular organization, network functionality, as well as cognitive and locomotor deficits were recently suggested to be pathological hallmarks in multiple sclerosis and corresponding animal models as they might occur following demyelination. To investigate functional changes following demyelination
Maria Nordheim Alme et al.
Journal of neuroimmunology, 285, 180-186 (2015-07-23)
Fingolimod (FTY720) is approved for treatment of relapsing-remitting multiple sclerosis. In vitro studies have found that fingolimod stimulates remyelination in cerebellar slices, but in vivo animal studies have not detected any positive effect on cerebral remyelination. The discrepant findings could
Hélène Jamann et al.
Frontiers in immunology, 13, 850616-850616 (2022-04-29)
Multiple sclerosis (MS) is characterized by the loss of myelin and of myelin-producing oligodendrocytes (OLs) in the central nervous system (CNS). Pro-inflammatory CD4+ Th17 cells are considered pathogenic in MS and are harmful to OLs. We investigated the mechanisms driving

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