Veli3 CRISPR/Cas9 KO Plasmid (m): sc-423669
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Veli3 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 Veli3 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 | |
Veli3 CRISPR/Cas9 KO Plasmid (m) | sc-423669 | 20 µg | $397.00 |
Overview
Lin7c encodes Veli3, a member of the LIN7 family of PDZ domain–containing scaffold proteins that organize membrane microdomains and couple transmembrane receptors to cytosolic signaling complexes. In mouse cells, Veli3 contributes to the assembly of polarity and junctional protein networks, influencing basolateral trafficking, receptor localization, and cytoskeletal organization. Through interactions with MAGUK and polarity regulators, LIN7C-associated complexes can modulate pathways that govern epithelial integrity, neuronal connectivity, and vesicle-mediated transport. Dysregulation of cell polarity and junctional scaffolding is linked to aberrant tissue architecture and altered signal transduction, making Lin7c a useful target for studying mechanisms relevant to developmental defects and disease-associated remodeling of cellular organization.
Veli3 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Lin7c gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Lin7c 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 Lin7c 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 Veli3 protein expression.
This CRISPR knockout system enables efficient generation of Lin7c-deficient cell models for investigation of Veli3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Lin7c exon(s) critical for Veli3 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 Lin7c genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Veli3 CRISPR/Cas9 KO Plasmid (m) and Veli3 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Lin7c locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Veli3 HDR Plasmid (m) and Veli3 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Lin7c homology arms to support homology-directed repair at defined Lin7c 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.