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MAB984

Sigma-Aldrich

Anti-Yellow Fever Virus Antibody, clone 2D12.A

ascites fluid, clone 2D12.A, Chemicon®

Synonym(s):

Yellow fever

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Pricing and availability is not currently available. Contact Technical Service

biological source

mouse

Quality Level

300

antibody form

ascites fluid

clone

2D12.A, monoclonal

species reactivity

human

manufacturer/tradename

Chemicon®

technique(s)

inhibition assay: suitable (hemagglutination)
neutralization: suitable

isotype

IgG2a

shipped in

wet ice

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technique(s)

cell culture | mammalian: suitable

technique(s)

cell culture | mammalian: suitable

technique(s)

cell culture | mammalian: suitable

technique(s)

cell culture | mammalian: suitable

recombinant

expressed in E. coli

recombinant

expressed in E. coli

recombinant

expressed in CHO cells

recombinant

expressed in bacteria

assay

≥95%

assay

≥95%

assay

≥95%

assay

≥95%

biological source

mouse

biological source

mouse

biological source

rat

biological source

rat

Quality Level

200

Quality Level

200

Quality Level

200

Quality Level

200

form

buffered aqueous solution

form

buffered aqueous solution

form

lyophilized powder

form

lyophilized powder

Specificity

Reacts with the envelope protein of the wild (Asibi) and vaccine strains of yellow fever virus. Preferentially neutralizes the Asibi strain. No cross-reactivity with other flaviviruses has been demonstrated.

Immunogen

17D strain of yellow virus.

Application

Neutralization (BLK) Asibi YF; 1:1000-1:3000.

Hemagglutination-inhibition: 1:3000-1:6000.
Research Category
Infectious Diseases
Research Sub Category
Infectious Diseases - Viral
This Anti-Yellow Fever Virus Antibody, clone 2D12.A is validated for use in HI, NEUT for the detection of Yellow Fever Virus.

Physical form

Ascites.

Storage and Stability

Maintain at -20°C for up to 12 months from date of receipt. Avoid repeated freeze/thaw cycles.

Legal Information

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

Disclaimer

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.

Storage Class Code

10 - Combustible liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Information

常规特殊物品
含少量动物源组分生物产品
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    Vasco Marcato et al.
    Molecular and cellular biology, 36(1), 13-29 (2015-10-16)
    Rapid upregulation of interferon beta (IFN-β) expression following virus infection is essential to set up an efficient innate antiviral response. Biological roles related to the antiviral and immune response have also been associated with the constitutive production of IFN-β in
    Patrick Ejlerskov et al.
    Cell, 163(2), 324-339 (2015-10-10)
    Neurodegenerative diseases have been linked to inflammation, but whether altered immunomodulation plays a causative role in neurodegeneration is not clear. We show that lack of cytokine interferon-β (IFN-β) signaling causes spontaneous neurodegeneration in the absence of neurodegenerative disease-causing mutant proteins.
    Judith van Holten et al.
    Arthritis research & therapy, 6(3), R239-R249 (2004-05-15)
    We investigated the therapeutic potential and mechanism of action of IFN-beta protein for the treatment of rheumatoid arthritis (RA). Collagen-induced arthritis was induced in DBA/1 mice. At the first clinical sign of disease, mice were given daily injections of recombinant
    Leesa M Pennell et al.
    Immunology, 152(3), 439-450 (2017-06-25)
    CD11c+ dendritic cells (DCs) exert a critical role as antigen-presenting cells in regulating pathogenic T cells in multiple sclerosis (MS). To determine whether the therapeutic benefit of interferon-β (IFN-β) treatment for MS is in part influenced by IFN regulation of
    ENU-induced mutation in USP18 causes hyperactivation of IFN-alphabeta signalling and suppresses STAT4-induced IFN-gamma production resulting in increased susceptibility to Salmonella Typhimurium
    Richer E, et al.
    Journal of immunology (Baltimore, Md. : 1950), 185(6), 3593-3593 (2010)
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