IFN-γRβ CRISPR/Cas9 KO Plasmid (h): sc-402794
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IFN-γRβ 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-γRβ 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-γRβ Antibody (A-11): sc-377291
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IFN-γRβ CRISPR/Cas9 KO Plasmid (h) | sc-402794 | 20 µg | $397.00 |
Overview
IFNGR2 encodes the interferon gamma receptor beta chain (IFN-γRβ), an essential co-receptor that pairs with IFNGR1 to form the functional IFN-γ receptor complex on the cell surface. Upon IFN-γ binding, IFN-γRβ supports activation of JAK1/JAK2 and downstream STAT1 signaling, driving transcriptional programs involved in antigen processing and presentation, macrophage activation, and antimicrobial immunity. This pathway interfaces with broader innate and adaptive immune networks, shaping inflammatory responses and immune surveillance. Genetic or functional disruption of IFNGR2 is linked to impaired IFN-γ responsiveness and susceptibility to severe infections, and altered signaling dynamics are relevant to studies of immune dysregulation and tumor–immune interactions.
IFN-γRβ CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the IFNGR2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the IFNGR2 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 IFNGR2 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-γRβ protein expression.
This CRISPR knockout system enables efficient generation of IFNGR2-deficient cell models for investigation of IFN-γRβ signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting IFNGR2 exon(s) critical for IFN-γRβ 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 IFNGR2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by IFN-γRβ CRISPR/Cas9 KO Plasmid (h) and IFN-γRβ CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the IFNGR2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by IFN-γRβ HDR Plasmid (h) and IFN-γRβ HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by IFNGR2 homology arms to support homology-directed repair at defined IFNGR2 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.