Description
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 1 bp deletion in exon 3 and 7 bp deletion in exon 3 and Insertion of the selection cassette in exon 3.,
Disease:Adenocarcinoma
Product details:
Knockout cell lysate achieved by CRISPR/Cas9.
REACH authorisation
Abcam has not and does not intend to apply for the REACH Authorisation of customers' uses of products that contain European Authorisation list (Annex XIV) substances.
It is the responsibility of our customers to check the necessity of application of REACH Authorisation, and any other relevant authorisations, for their intended uses.
Lysate preparation:
Our lysates are made using RIPA buffer to which we add a protease inhibitor cocktail and phosphatase inhibitor cocktail (ratio: 300:100:10).
This means that the protein of interest is denatured.
If you require a native form of the protein please use the live cell version. Please refer to our lysis protocol for further details on how our lysates are prepared.
User storage instructions:
Lyophilizate may be stored at 4°C. After reconstitution, store at -20°C for short-term storage or -80°C for long-term storage.
This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our
limited use license
patent pages
Properties and Storage Information:
Gene name-IVNS1ABP, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Shipped at conditions-Ambient - Can Ship with Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
Influenza Virus NS1A Binding Protein (IVNS1ABP) also known as NS1-BP is a cellular protein that interacts with the NS1 protein of the influenza virus to modulate viral replication. This interaction suppresses host antiviral responses enhancing influenza virus propagation. IVNS1ABP has a molecular weight of approximately 77 kDa. It expresses mainly in the nucleus and cytoplasm of host cells where it engages with host molecules to facilitate viral protein synthesis and assembly.
Biological function summary
IVNS1ABP contributes to the regulation of protein synthesis pathways and facilitates RNA processing by directly interacting with host machinery. It functions within a complex containing several host proteins that assist in transcriptional control and mRNA splicing. These interactions provide the influenza virus with a supportive environment for efficient propagation effectively avoiding the host's immune defenses.
Pathways
IVNS1ABP operates in the RNA processing and splicing mechanisms that are critical for both host and viral gene expression. The protein forms pathways with host RNA polymerase II and other spliceosomal components influencing the maturation of mRNA precursors. These pathways not only support viral replication but also adjust host cell pathways to prioritize viral transcription over normal cellular processes.
IVNS1ABP's modification of host defenses links it directly to influenza pathogenesis and secondary immune suppression. This protein also connects to the nonstructural NS1 protein of the influenza virus an interaction important for evading the host immune response. Understanding IVNS1ABP's role in these pathways helps develop therapeutic strategies for controlling influenza infections targeting its interactions to hinder the viral lifecycle.
