Anti-Influenza A virus NS1 protein antibody [EPR28247-51],Abcam,AB313341

Patented technology Our RabMAb ® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb ® patents . 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 .

Host

Rabbit

Reactivity

Influenza A

Application

WB, IHC-P, Flow Cyt (Intra), ICC/IF, I-ELISA

Platform ID

BAB918004877

Abcam

Headquarters

Discovery Drive Cambridge Biomedical Campus Cambridge CB2 0AX UK

Contact

Tel: +44 (0)1223 696000
Fax: +44 (0)1223 215 215

Product Specifications
Scientific Background

Specifications

NameAnti-Influenza A virus NS1 protein antibody [EPR28247-51]
Cat. No.AB313341
HostRabbit
IsotypeIgG
ReactivityInfluenza A
ApplicationWB, IHC-P, Flow Cyt (Intra), ICC/IF, I-ELISA
ClonalityMonoclonal
Clone NumberEPR28247-51
Concentration0.5 mg/mL Batch dependent concentration
ImmunogenThe exact immunogen used to generate this antibody is proprietary information.
PurityAffinity purification Protein A
Appearance/FormLiquid
ShippingBlue Ice
FormulationpH: 7.2 - 7.4 Preservative: 0.01% Sodium azide Constituents: PBS, 40% Glycerol (glycerin, glycerine), 0.05% BSA
Storage-20°C
Regulatory StatusResearch Use Only

Scientific Background

Target data Inhibits post-transcriptional processing of cellular pre-mRNA, by binding and inhibiting two cellular proteins that are required for the 3'-end processing of cellular pre-mRNAs : the 30 kDa cleavage and polyadenylation specificity factor/CPSF4 and the poly(A)-binding protein 2/PABPN1. In turn, unprocessed 3' end pre-mRNAs accumulate in the host nucleus and are no longer exported to the cytoplasm. Cellular protein synthesis is thereby shut off very early after virus infection. Viral protein synthesis is not affected by the inhibition of the cellular 3' end processing machinery because the poly(A) tails of viral mRNAs are produced by the viral polymerase through a stuttering mechanism. Prevents the establishment of the cellular antiviral state by inhibiting TRIM25-mediated RIGI ubiquitination, which normally triggers the antiviral transduction signal that leads to the activation of type I IFN genes by transcription factors IRF3 and IRF7. Also binds poly(A) and U6 snRNA. Inhibits the integrated stress response (ISR) in the infected cell by blocking dsRNA binding by EIF2AK2/PKR and further phosphorylation of EIF2S1/EIF-2ALPHA (PubMed : 33766561). Stress granule formation is thus inhibited, which allows protein synthesis and viral replication (PubMed : 33766561). See full target information NS

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