IFN-ω CRISPR/Cas9 KO Plasmid (h): sc-409162
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IFN-omega CRISPR/Cas9 Knockout (KO) Plasmid (h) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the IFN-omega genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: IFN-ω Antibody (1PL11): sc-71318
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IFN-ω CRISPR/Cas9 KO Plasmid (h) | sc-409162 | 20 µg | $397.00 |
Overview
IFNW1 encodes interferon-omega (IFN-ω), a type I interferon cytokine that contributes to innate antiviral defense and immune regulation. Upon engagement of the IFNAR receptor complex, IFN-ω activates JAK1/TYK2-dependent signaling to induce STAT1/STAT2/IRF9-driven transcription of interferon-stimulated genes (ISGs), shaping antiviral restriction, antigen presentation, and inflammatory tone. This pathway intersects with IRF and NF-κB programs to coordinate pathogen sensing responses and crosstalk with adaptive immunity. Dysregulated type I interferon signaling is implicated in viral susceptibility, chronic inflammation, and interferon-associated autoimmune phenotypes, making IFNW1 a useful node for dissecting interferon biology.
IFN-omega CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the IFNW1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the IFNW1 together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the IFNW1 open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish IFN-omega protein expression.
This CRISPR knockout system enables efficient generation of IFNW1-deficient cell models for investigation of IFN-omega signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting IFNW1 exon(s) critical for IFN-omega function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple IFNW1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by IFN-omega CRISPR/Cas9 KO Plasmid (h) and IFN-omega CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the IFNW1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by IFN-omega HDR Plasmid (h) and IFN-omega HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by IFNW1 homology arms to support homology-directed repair at defined IFNW1 target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.