Wnt-3a CRISPR/Cas9 KO Plasmid (m): sc-423716
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Wnt-3a 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 Wnt-3a 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: Wnt-3a Antibody (3A6): sc-136163
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Wnt-3a CRISPR/Cas9 KO Plasmid (m) | sc-423716 | 20 µg | $397.00 |
Overview
Mouse Wnt3a encodes the secreted glycoprotein Wnt-3a, a key ligand in canonical Wnt/β-catenin signaling that regulates embryonic patterning, stem cell maintenance, and tissue morphogenesis. Wnt-3a binding to Frizzled/LRP receptors stabilizes β-catenin, enabling TCF/LEF-dependent transcriptional programs that coordinate proliferation, differentiation, and cell fate decisions. In addition to roles in development, Wnt3a activity intersects with pathways controlling epithelial–mesenchymal dynamics, organogenesis, and regenerative responses. Dysregulated Wnt-3a signaling is frequently studied in contexts of aberrant β-catenin signaling, including oncogenic transformation and developmental defects, making it a central node for pathway and mechanism research.
Wnt-3a CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Wnt3a gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Wnt3a 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 Wnt3a 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 Wnt-3a protein expression.
This CRISPR knockout system enables efficient generation of Wnt3a-deficient cell models for investigation of Wnt-3a signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Wnt3a exon(s) critical for Wnt-3a 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 Wnt3a genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Wnt-3a CRISPR/Cas9 KO Plasmid (m) and Wnt-3a CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Wnt3a locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Wnt-3a HDR Plasmid (m) and Wnt-3a HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Wnt3a homology arms to support homology-directed repair at defined Wnt3a 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.