Recombinant Influenza A virus Non-structural protein 1 (NS)

Product Description

Recombinant Influenza A virus Non-structural protein 1 (NS) is available at Gentaur for Next week Delivery.

Gene Name: NS

Alternative Names : NS1A

Expression Region : 1-237aa

AA Sequence : MDPNTVSSFQVDCFLWHVRKRVADQELGDAPFLDRLRRDQKSLKGRGSTLGLNIETATRVGKQIVERILKEESDEALKMTMASAPASRYLTDMTIEEMSRDWFMLMPKQKVAGPLCIRMDQAVMDKSIILKANFSVIFDRLETLILLRAFTEEGAIVGEISPLPSLPGHTNEDVKNAIGVLIGGLEWNDNTVRVSKTLQRFAWRSSNENGGPPLTPKQKRKMARTIRSEVRRNKMVD

Sequence Info : Full Length

Tag Info : N-terminal 6xHis-tagged

Theoretical MW : 28.8 kDa

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-

Biological Activity : Not tested

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

Research Area : Microbiology

Restriction : For Research Use Only. Not for use in diagnostic procedures, drug use, or for administration to humans or animals.

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.

Involvement in disease :

Subcellular location : Host nucleus, Host cytoplasm

Protein Families : Influenza A viruses NS1 family

Tissue Specificity :

Paythway :

Uniprot ID : Q0HD54