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The antibody against NS was raised in rabbit using the Recombinant Influenza A virus Non-structural protein 1 protein (1-237AA) as the immunogen. This antibody exists as a non-conjugated isotype IgG, purified by protein G with a purity greater than 95%. This antibody has been validated on ELISA, WB.
The antibody against NS was raised in rabbit using the Recombinant Influenza A virus Non-structural protein 1 protein (1-237AA) as the immunogen. This antibody exists as a non-conjugated isotype IgG, purified by protein G with a purity greater than 95%. This antibody has been validated on ELISA, WB.
$299.00
| Cat.No | ADC-02573A | Clonality | Polyclonal |
|---|---|---|---|
| Host Species | Rabbit | Target Name | NS |
| Target Synonyms | NS antibody; Non-structural protein 1 antibody; NS1 antibody; NS1A antibody | Form | Liquid |
| Species Reactivity | Influenza A virus | Isotype | IgG |
| Storage Buffer | 0.01M PBS, 0.03% Proclin 300; Constituents: 50% Glycerol, PH 7.4 | Purification Method | >95%, Protein G purified |
| Conjugate | Non-conjugated | Application | ELISA, WB |
| Storage | Upon receipt |
| Immunogen Description | Recombinant Influenza A virus Non-structural protein 1 protein (1-237AA) | Target Species | Influenza A virus |
|---|---|---|---|
| Immunogen Sequence | Complete sequences for the immunogen, target protein, and peptides are available upon request. | Uniprot ID | Q0HD54 |
Uniprot Id
Q0HD54
Target Species
Influenza A virus
Target Name
NS
Target Function
Prevents the establishment of the cellular antiviral state by inhibiting TRIM25-mediated DDX58 ubiquitination, which normally triggers the antiviral transduction signal that leads to the activation of type I IFN genes by transcription factors IRF3 and IRF7. Prevents human EIF2AK2/PKR activation, either by binding double-strand RNA, or by interacting directly with EIF2AK2/PKR. This function may be important at the very beginning of the infection, when NS1 is mainly present in the cytoplasm. Also binds poly(A) and U6 snRNA.; 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.
Target Subcellular Location
Host nucleus. Host cytoplasm.
Target Protein Families
Influenza A viruses NS1 family
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