IFI-203 CRISPR/Cas9 KO Plasmid (m): sc-421032
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IFI-203 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 IFI-203 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 | |
IFI-203 CRISPR/Cas9 KO Plasmid (m) | sc-421032 | 20 µg | $397.00 |
Overview
Ifi203 encodes IFI-203, a mouse interferon-inducible protein implicated in innate immune surveillance and regulation of inflammatory gene programs. IFI-203 is commonly studied in the context of interferon-stimulated responses, where it can influence nucleic-acid sensing, transcriptional control, and downstream cytokine signaling. Altered regulation of interferon pathways is relevant to models of autoimmunity, chronic inflammation, and host–pathogen interactions, making Ifi203 a useful locus for dissecting cell-intrinsic immune circuitry. Loss- or gain-of-function perturbation of Ifi203 can help define how interferon-driven programs shape immune cell activation states and tissue inflammatory phenotypes in mice.
IFI-203 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ifi203 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ifi203 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 Ifi203 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 IFI-203 protein expression.
This CRISPR knockout system enables efficient generation of Ifi203-deficient cell models for investigation of IFI-203 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ifi203 exon(s) critical for IFI-203 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 Ifi203 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by IFI-203 CRISPR/Cas9 KO Plasmid (m) and IFI-203 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ifi203 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by IFI-203 HDR Plasmid (m) and IFI-203 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ifi203 homology arms to support homology-directed repair at defined Ifi203 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.