Product Description
Size: 20µg / 100µg / 1mg
Mouse Recombinant Monoclonal N1, influenza A H1N1, A/Brisbane/59/2007 antibody. Suitable for ICC/IF, I-ELISA and reacts with Transfected cell line - Influenza A virus (A/Brisbane/59/2007(H1N1)), Recombinant full length protein - Influenza A virus (A/Brisbane/59/2007(H1N1)) samples.
Key facts
Host species:Mouse,
Clonality:Monoclonal,
Clone number:3A2,
Isotype:IgG2a,
Carrier free:No,
Reacts with:Influenza A virus (A/Brisbane/59/2007(H1N1)),
Applications:I-ELISA, ICC/IFSee reactivity dataSee the reactivity data table below for information on validated species and application combinations.,
Immunogen:The exact immunogen used to generate this antibody is proprietary information.,
Specificity:This antibody reacts with Influenza A virus H1N1, A/Brisbane/59/2007 neuraminidase and does not react with Influenza A virus H1N1, A/California/07/2009 neuraminidase or Influenza A virus H7N9, A/Anhui/1/2013 neuraminidase.
Product details:
What are the advantages of a recombinant monoclonal antibody?
This product is a recombinant monoclonal antibody, which offers several advantages including:
- High batch-to-batch consistency and reproducibility
- Improved sensitivity and specificity
- Long-term security of supply
- Animal-free batch production
For more information, read more on
recombinant antibodies
Want a custom formulation?
This antibody clone is manufactured by Abcam. If you require a custom buffer formulation or conjugation for your experiments, please contact orders@abcam.com
Properties and Storage Information:
Form-Liquid, Purification technique-Affinity purification Protein A, Storage buffer-pH: 7.2 - 7.4Preservative: 0.01% Sodium azideConstituents: PBS, 40% Glycerol (glycerin, glycerine), 0.05% BSA, Shipped at conditions-Blue Ice, Appropriate short-term storage duration-1-2 weeks, Appropriate short-term storage conditions-+4°C, Appropriate long-term storage conditions--20°C, Aliquoting information-Upon delivery aliquot, Storage information-Avoid freeze / thaw cycle
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
Influenza A H1N1 (A/Brisbane/59/2007) neuraminidase also known as NA plays an important role mechanically in the viral life cycle. This enzyme facilitates the release of viral particles from infected host cells by cleaving sialic acid residues from glycoproteins. NA has an approximate molecular weight of 60 kDa and is expressed on the surface of influenza viral particles. Neuraminidase works closely with hemagglutinin (HA) another surface glycoprotein to ensure efficient viral budding and spread.
Biological function summary
Influenza A H1N1 neuraminidase contributes significantly to the virus's replication and transmission. As part of the viral envelope NA aids in the detachment of newly formed virions from the host cell surface. It operates as a homotetramer meaning it forms a complex with four identical subunits to execute its enzymatic activity. The neuraminidase protein is critical for overcoming the host's mucosal barriers facilitating infection of respiratory epithelial cells.
Pathways
Neuraminidase from the H1N1 influenza strain is directly involved in the viral replication cycle. The two main pathways where NA functions are the influenza virus life cycle and viral entry into host cells. In these pathways neuraminidase acts in tandem with hemagglutinin (HA) to mediate the initial host cell entry and subsequent virus spread making it a focal point for vaccine and antiviral drug development.
Influenza A H1N1 neuraminidase associates closely with influenza infection a significant cause of respiratory illness globally. The NA protein also plays a role in the pathogenesis of pandemic influenza marked by rapid spread and high morbidity. In this context neuraminidase inhibitors such as oseltamivir target NA to disrupt its function and curb the infection. Additionally research connects neural cell adhesion molecule (NCAM) to influenza pathogenesis highlighting the complex interactions between viral proteins and host cell receptors that contribute to disease progression.
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Collaboration
Tony Tang
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