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Recombinant Influenza A virus Non-structural protein 1 (NS), Cat#RPC22952

$438.00

Cat#

RPC22952

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Species

Influenza A virus (strain A/Hickox/1940 H1N1)

Source

E.coli

Tag Info

N-terminal 6xHis-tagged

Biological Activity

Not tested

Estimated Turnaround Time

15-25 business days

Gene Name

NS

Alternative Names

NS1A

Uniprot

Q0HD54

Expression Region

1-237aa

AA Sequence

MDPNTVSSFQVDCFLWHVRKRVADQELGDAPFLDRLRRDQKSLKGRGSTLGLNIETATRVGKQIVERILKEESDEALKMTMASAPASRYLTDMTIEEMSRDWFMLMPKQKVAGPLCIRMDQAVMDKSIILKANFSVIFDRLETLILLRAFTEEGAIVGEISPLPSLPGHTNEDVKNAIGVLIGGLEWNDNTVRVSKTLQRFAWRSSNENGGPPLTPKQKRKMARTIRSEVRRNKMVD

Sequence Info

Full Length

Theoretical MW

30.8 kDa

Purity

>85% as determined by SDS-PAGE.

Storage Buffer

Tris/PBS-based buffer, 5%-50% glycerol. If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.

Endotoxin Level

Not tested

Shipping Condition

Ice packs

Storage

Short term: -20°C; Long term: -80°C. Minimize freeze and thaw cycles.

Expiry Date

1 year

Research Area

Microbiology

Restriction

For Research Use Only. Not for use in diagnostic procedures. Not for human or animal drug or food use.

Relevance

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 30KDA 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.

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.

Subcellular location

Host nucleus, Host cytoplasm

Protein Families

Influenza A viruses NS1 family

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