FRP-3 CRISPR/Cas9 KO Plasmid (m): sc-422898
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FRP-3 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 FRP-3 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: FRP-3 Antibody (B-5): sc-514350
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FRP-3 CRISPR/Cas9 KO Plasmid (m) | sc-422898 | 20 µg | $397.00 |
Overview
Frzb encodes FRP-3 (also known as secreted frizzled-related protein 3), an extracellular modulator of Wnt signaling that binds Wnt ligands and can attenuate Frizzled receptor activation. By shaping canonical β-catenin–dependent transcription and non-canonical Wnt pathways, FRP-3 contributes to regulation of embryonic patterning, tissue morphogenesis, and mesenchymal lineage differentiation, including skeletal and cartilage homeostasis. In mouse models, altered FRP-3 activity has been associated with changes in bone formation dynamics and extracellular matrix remodeling, processes frequently linked to developmental abnormalities and degenerative phenotypes. Because Wnt signaling is tightly coupled to cell fate decisions and proliferative control, Frzb is widely studied in contexts where pathway imbalance contributes to inflammation-associated tissue remodeling and tumor biology.
FRP-3 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Frzb gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Frzb 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 Frzb 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 FRP-3 protein expression.
This CRISPR knockout system enables efficient generation of Frzb-deficient cell models for investigation of FRP-3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Frzb exon(s) critical for FRP-3 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 Frzb genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by FRP-3 CRISPR/Cas9 KO Plasmid (m) and FRP-3 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Frzb locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by FRP-3 HDR Plasmid (m) and FRP-3 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Frzb homology arms to support homology-directed repair at defined Frzb 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.