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Influenza A H1N1 (strain A/Malaysia:Malaya/302/1954) Non-structural protein 1 (His & Myc)

Catalog No. TMPH-02349

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.

All products from TargetMol are for Research Use Only. Not for Human or Veterinary or Therapeutic Use.
Influenza A H1N1 (strain A/Malaysia:Malaya/302/1954) Non-structural protein 1 (His & Myc)
Pack Size Availability Price/USD Quantity
20 μg 20 days $ 360.00
100 μg 20 days $ 678.00
1 mg 20 days $ 2,300.00
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Biological Description
Technical Params
Product Properties
Description 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.
Species H1N1
Expression System E. coli
Tag N-10xHis, C-Myc
Accession Number A4K149
Amino Acid MDPNTVSSFQVDCFLWHVRKQVADQELGDAPFLDRLRRDQKSLRGRGSTLGLNIETATRVGKQIVERILKEESDEALKMTMASAPASRYLTDMTIEEMSRDWFMLMPKQKVAGPLCIRMDQAIMDKNIILKANFSVIFDRLETLILLRAFTEEGAIVGEISPLPSLPGHTNEDVKNAIGVLIGGLEWNDNTVRVSKTLQRFAWRSSNENGRPPLTPKQKRKMARTIRSEVRRNKMAD
Construction 1-237 aa
Protein Purity > 85% as determined by SDS-PAGE.
Molecular Weight 34.4 kDa (predicted)
Formulation Tris-based buffer, 50% glycerol
Reconstitution A Certificate of Analysis (CoA) containing reconstitution instructions is included with the products. Please refer to the CoA for detailed information.
Stability & Storage

Lyophilized powders can be stably stored for over 12 months, while liquid products can be stored for 6-12 months at-80℃. For reconstituted proteinsolutions, the solution can be stored at -20°c to -80'c for at least 3 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.
Shipping

In general, Lyophilized powders are shipping with blue ice. Solutions are shipping with dry ice.
Research Background 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.

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Keywords

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