IFN-αB CRISPR/Cas9 KO Plasmid (m): sc-421046
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IFN-αB 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-αB 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-αB CRISPR/Cas9 KO Plasmid (m) | sc-421046 | 20 µg | $397.00 |
Overview
Mouse Ifnab encodes interferon-αB (IFN-αB), a type I interferon that amplifies innate antiviral defenses and shapes subsequent adaptive immune responses. Upon pattern-recognition receptor signaling through pathways such as cGAS–STING, RIG-I/MDA5–MAVS, and endosomal TLRs, IFN-αB engages IFNAR to activate JAK–STAT signaling and drive transcription of interferon-stimulated genes that modulate antigen presentation, apoptosis, and inflammatory cytokine networks. Dysregulated type I interferon activity is implicated in chronic inflammation and autoimmunity, and altered interferon signatures are frequently examined in models of viral infection and immune-mediated pathology. Ifnab function is therefore relevant to studies of host–pathogen interactions, myeloid and lymphoid cell programming, and interferon-driven tissue responses.
IFN-αB CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ifnab gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ifnab 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 Ifnab 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-αB protein expression.
This CRISPR knockout system enables efficient generation of Ifnab-deficient cell models for investigation of IFN-αB signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ifnab exon(s) critical for IFN-αB 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 Ifnab genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by IFN-αB CRISPR/Cas9 KO Plasmid (m) and IFN-αB CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ifnab locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by IFN-αB HDR Plasmid (m) and IFN-αB HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ifnab homology arms to support homology-directed repair at defined Ifnab 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.