Wnt-7b CRISPR/Cas9 KO Plasmid (m): sc-423722
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Wnt-7b 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-7b 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 | |
Wnt-7b CRISPR/Cas9 KO Plasmid (m) | sc-423722 | 20 µg | $397.00 |
Overview
Wnt7b encodes the secreted glycoprotein Wnt-7b, a ligand that activates canonical and non-canonical Wnt signaling to regulate cell fate decisions, proliferation, polarity, and tissue patterning during embryogenesis and postnatal homeostasis in mouse. Wnt-7b engagement of Frizzled/LRP receptors influences β-catenin–dependent transcription as well as planar cell polarity and Ca²⁺-linked pathways, shaping epithelial–mesenchymal interactions and organ morphogenesis. Dysregulated Wnt7b activity has been linked to aberrant developmental programs and remodeling processes that intersect with oncogenic signaling, fibrosis, and inflammatory microenvironments in multiple tissue contexts. As a pathway node, Wnt-7b is frequently studied for its roles in stem/progenitor cell behavior, vascular and airway biology, and crosstalk with TGF-β, Hedgehog, and Notch signaling.
Wnt-7b CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Wnt7b gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Wnt7b 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 Wnt7b 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-7b protein expression.
This CRISPR knockout system enables efficient generation of Wnt7b-deficient cell models for investigation of Wnt-7b signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Wnt7b exon(s) critical for Wnt-7b 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 Wnt7b genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Wnt-7b CRISPR/Cas9 KO Plasmid (m) and Wnt-7b CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Wnt7b locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Wnt-7b HDR Plasmid (m) and Wnt-7b HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Wnt7b homology arms to support homology-directed repair at defined Wnt7b 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.