SARP3 CRISPR/Cas9 KO Plasmid (m): sc-424898
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SARP3 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 SARP3 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: SARP3 Antibody (H-6): sc-374397
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SARP3 CRISPR/Cas9 KO Plasmid (m) | sc-424898 | 20 µg | $397.00 |
Overview
Sfrp5 encodes SARP3, a secreted frizzled-related protein that modulates extracellular Wnt ligand availability and fine-tunes Wnt/β-catenin and non-canonical Wnt signaling. By shaping receptor–ligand interactions at the cell surface, SARP3 influences cell fate specification, proliferation, and tissue remodeling during development and in adult homeostasis. In mouse models, altered Sfrp5 activity has been linked to dysregulated adipose biology, inflammation, and metabolic phenotypes, making it relevant to studies of insulin sensitivity and energy balance. Its secreted nature also positions SARP3 as a key node in paracrine signaling within stromal–immune–epithelial microenvironments.
SARP3 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Sfrp5 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Sfrp5 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 Sfrp5 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 SARP3 protein expression.
This CRISPR knockout system enables efficient generation of Sfrp5-deficient cell models for investigation of SARP3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Sfrp5 exon(s) critical for SARP3 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 Sfrp5 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SARP3 CRISPR/Cas9 KO Plasmid (m) and SARP3 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Sfrp5 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SARP3 HDR Plasmid (m) and SARP3 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Sfrp5 homology arms to support homology-directed repair at defined Sfrp5 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.