Abcam, ab257807, Human ZC3HAV1 (Zinc finger antiviral protein) knockout A549 cell lysate

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ZC3HAV1 KO cell lysate available now. KO validated by. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon4 and 2 bp insertion in exon4.
Key facts
Cell type:A549,
Species or organism:Human,
Tissue:Lung,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon4 and 2 bp insertion in exon4.,
Disease:Carcinoma

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-ZC3HAV1, 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.
Zinc finger antiviral protein (ZAP) also known as zinc antiviral is a cellular protein that plays an important role in antiviral defense. ZAP recognizes and binds to the CpG dinucleotide-rich regions of viral RNA targeting them for degradation and preventing viral replication. This protein has a molecular mass of around 100 kDa and is encoded by the ZC3HAV1 gene. ZAP predominantly expresses in the cytoplasm of various cells notably in immune cells where it carries out its antiviral function against a wide range of viruses.
Biological function summary
Zinc finger antiviral protein serves a critical role in the innate immune response. ZAP is part of a complex involving several cofactors that facilitate its antiviral activity. This protein collaborates with TRIM25 and AGO2 to recruit RNA degradation machinery targeting viral mRNA for decay. ZAP's interactions highlight its importance in the cellular response to viral infection making it an attractive target for developing antiviral therapies.
Pathways
Zinc finger antiviral protein is integral to the interferon signaling and viral RNA degradation pathways. Interferon signaling initiates the expression of ZAP linking it with other interferon-stimulated genes to enhance the antiviral response. Within the RNA degradation pathway ZAP coordinates with proteins like TRIM25 augmenting the destruction of viral genetic material. These pathways highlight the protein's role in suppressing viral replication and promoting cell survival during infections.
Zinc finger antiviral protein plays a significant role in conditions associated with viral infections and autoimmune disorders. ZAP confers protection against diseases like Hepatitis B and C by inhibiting viral RNA. Apart from infectious diseases ZAP interacts with proteins like HRAS and IRF3 suggesting its involvement in autoimmune conditions where viral components trigger immune responses. This relationship opens possibilities for therapeutic intervention by modulating ZAP activity in disease contexts.