Anti-West Nile/dengue virus E protein Antibody (E60)
Anti-West Nile/dengue virus E protein Antibody (E60) is mouse-derived IgG2a κ type antibody inhibitor, targeting to West Nile/dengue virus E protein. Anti-West Nile/dengue virus E protein Antibody (E60) can cross-neutralize West Nile virus (WNV) and dengue virus (DENV) envelope (E) protein. Anti-West Nile/dengue virus E protein Antibody (E60) can be used for the researches of WNV and DENV infection.
For research use only. We do not sell to patients.
- Molecular Weight:150 kDa
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Isotype
Mouse IgG2a kappa
Recommend Isotype Controls
Species Reactivity
Virus
IC50 & Target
West Nile/dengue virus E protein
In Vitro
Anti-West Nile/dengue virus E protein Antibody (E60) (1 h) increases neutralization with dengue virus (DENV) than West Nile virus (WNV)[1].
Anti-West Nile/dengue virus E protein Antibody (E60) (10 μg/mL, 16 h) displays limited neutralization of WT Zika virus (ZIKV) reporter virus particles (RVPs)[2].
Anti-West Nile/dengue virus E protein Antibody (E60) completely neutralizes mature RVP preparations of ZIKV containing either the DENV1 or DENV2 loop, with EC50 of 64.4 and 176.6 ng/mL, respectively[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Conjugated
Unconjugated
Reconsititution
The product can be reconstituted/diluted with sterile PBS or saline.
Format
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Product Image
Application
Neutralization of WNV; Neutralization of DENV1,2,3,4
Chemical Information
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Molecular Weight 150 kDa
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SMILES
[Anti-West Nile/dengue virus E protein Antibody (E60)]
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Formulation
Please refer to the lot-specific COA for specific buffer information.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
Purity & Documentation
References
[1]. Dowd KA, et al. A dynamic landscape for antibody binding modulates antibody-mediated neutralization of West Nile virus. PLoS Pathog. 2011 Jun;7(6):e1002111. [Content Brief]
[2]. Goo L, et al. The Zika virus envelope protein glycan loop regulates virion antigenicity. Virology. 2018 Feb;515:191-202. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)