ZNRF3 CRISPR/Cas9 KO Plasmid (h): sc-418162
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ZNRF3 CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 ZNRF3 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 | |
ZNRF3 CRISPR/Cas9 KO Plasmid (h) | sc-418162 | 20 µg | $397.00 |
Overview
ZNRF3 (zinc and ring finger 3) encodes a transmembrane E3 ubiquitin ligase that acts as a negative feedback regulator of Wnt/β-catenin signaling by promoting ubiquitination and turnover of Frizzled and LRP5/6 receptor complexes at the cell surface. Through interactions with R-spondins and LGR receptors, ZNRF3 helps calibrate pathway amplitude, influencing stem cell maintenance, tissue homeostasis, and differentiation programs. Disruption of ZNRF3-mediated receptor regulation can potentiate Wnt signaling and alter transcriptional outputs controlling proliferation and lineage commitment. Genetic and functional alterations in ZNRF3 have been implicated in Wnt-dependent disease biology, making it a useful node for mechanistic studies of pathway control.
ZNRF3 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the ZNRF3 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the ZNRF3 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 ZNRF3 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 ZNRF3 protein expression.
This CRISPR knockout system enables efficient generation of ZNRF3-deficient cell models for investigation of ZNRF3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting ZNRF3 exon(s) critical for ZNRF3 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 ZNRF3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ZNRF3 CRISPR/Cas9 KO Plasmid (h) and ZNRF3 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the ZNRF3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ZNRF3 HDR Plasmid (h) and ZNRF3 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by ZNRF3 homology arms to support homology-directed repair at defined ZNRF3 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.