IFN-α5 CRISPR/Cas9 KO Plasmid (m): sc-421042
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IFN-α5 CRISPR/Cas9 Knockout (KO) Plasmid (m) 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-α5 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
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IFN-α5 CRISPR/Cas9 KO Plasmid (m) | sc-421042 | 20 µg | $397.00 |
Overview
Mouse Ifna5 encodes interferon‑α5 (IFN‑α5), a type I interferon that coordinates innate antiviral defenses and shapes downstream adaptive immune responses. IFN‑α5 signals through the IFNAR receptor complex to activate JAK–STAT pathways, inducing interferon‑stimulated genes that restrict viral replication, modulate antigen presentation, and regulate cell survival programs. This cytokine axis influences inflammatory tone in tissues and intersects with pattern‑recognition receptor signaling, including RIG‑I/MAVS and cGAS–STING pathways. Dysregulated type I interferon signaling is implicated in infection susceptibility and in immune‑mediated inflammatory phenotypes relevant to autoimmunity and tumor immune microenvironments.
IFN-α5 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ifna5 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ifna5 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 Ifna5 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-α5 protein expression.
This CRISPR knockout system enables efficient generation of Ifna5-deficient cell models for investigation of IFN-α5 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ifna5 exon(s) critical for IFN-α5 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 Ifna5 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by IFN-α5 CRISPR/Cas9 KO Plasmid (m) and IFN-α5 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ifna5 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by IFN-α5 HDR Plasmid (m) and IFN-α5 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ifna5 homology arms to support homology-directed repair at defined Ifna5 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.