FPR2 CRISPR/Cas9 KO Plasmid (m): sc-420405
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FPR2 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 FPR2 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 | |
FPR2 CRISPR/Cas9 KO Plasmid (m) | sc-420405 | 20 µg | $397.00 |
Overview
Formyl peptide receptor 2 (FPR2; gene Fpr2) is a mouse G protein–coupled receptor that recognizes diverse chemoattractant and pro-resolving ligands, coupling to Gi signaling to regulate leukocyte chemotaxis, adhesion, and activation. FPR2 engagement modulates downstream pathways including PI3K/AKT, MAPK/ERK, PLCβ-driven calcium mobilization, and β-arrestin–associated signaling, shaping inflammatory mediator release and reactive oxygen species responses. Through these programs, FPR2 contributes to innate immune surveillance and resolution biology, with documented relevance to inflammatory tissue injury, infection-associated inflammation, and immune-driven pathology. Its context-dependent signaling makes it a useful target for dissecting how GPCR inputs reprogram myeloid cell behavior across inflammatory microenvironments.
FPR2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Fpr2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Fpr2 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 Fpr2 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 FPR2 protein expression.
This CRISPR knockout system enables efficient generation of Fpr2-deficient cell models for investigation of FPR2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Fpr2 exon(s) critical for FPR2 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 Fpr2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by FPR2 CRISPR/Cas9 KO Plasmid (m) and FPR2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Fpr2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by FPR2 HDR Plasmid (m) and FPR2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Fpr2 homology arms to support homology-directed repair at defined Fpr2 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.