FRP-4 CRISPR/Cas9 KO Plasmid (m): sc-422899
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FRP-4 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-4 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 | |
FRP-4 CRISPR/Cas9 KO Plasmid (m) | sc-422899 | 20 µg | $397.00 |
Overview
Sfrp4 encodes secreted frizzled-related protein 4 (FRP-4), a soluble modulator of Wnt signaling that binds Wnt ligands and/or Frizzled receptors to tune β-catenin–dependent and non-canonical pathway output. In mouse tissues, FRP-4 contributes to regulation of cell fate decisions, proliferation, extracellular matrix remodeling, and differentiation programs important for developmental patterning and tissue homeostasis. Altered Sfrp4 expression has been associated with dysregulated Wnt pathway activity in contexts such as fibrosis, metabolic tissue remodeling, and tumor biology, where shifts in Wnt tone can impact epithelial–mesenchymal interactions and stromal responses. As a secreted pathway regulator, Sfrp4 is frequently studied in signaling cross-talk networks that integrate Wnt with TGF-β, inflammatory cues, and lineage-specifying transcriptional programs.
FRP-4 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Sfrp4 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Sfrp4 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 Sfrp4 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-4 protein expression.
This CRISPR knockout system enables efficient generation of Sfrp4-deficient cell models for investigation of FRP-4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Sfrp4 exon(s) critical for FRP-4 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 Sfrp4 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by FRP-4 CRISPR/Cas9 KO Plasmid (m) and FRP-4 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Sfrp4 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by FRP-4 HDR Plasmid (m) and FRP-4 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Sfrp4 homology arms to support homology-directed repair at defined Sfrp4 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.