VILL CRISPR/Cas9 KO Plasmid (m): sc-423675
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- VILL 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 VILL 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 | |
VILL CRISPR/Cas9 KO Plasmid (m) | sc-423675 | 20 µg | $397.00 |
Overview
Vill encodes villin-like (VILL), an actin-binding cytoskeletal protein enriched in epithelial contexts where it contributes to organization and remodeling of F-actin networks. Proteins in the villin/gelsolin superfamily regulate actin filament severing, bundling, and stabilization, linking calcium and phosphoinositide cues to changes in cell shape, polarity, and barrier-associated architecture. Through these roles, VILL is relevant to pathways governing epithelial differentiation, microvillar organization, and dynamic junctional remodeling that influence tissue homeostasis. Dysregulated actin dynamics and epithelial structural integrity are broadly implicated in inflammation, barrier dysfunction, and tumor-associated remodeling, making Vill a useful locus for mechanistic studies of cytoskeletal control.
VILL CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Vill gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Vill 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 Vill 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 VILL protein expression.
This CRISPR knockout system enables efficient generation of Vill-deficient cell models for investigation of VILL signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Vill exon(s) critical for VILL 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 Vill genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by VILL CRISPR/Cas9 KO Plasmid (m) and VILL CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Vill locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by VILL HDR Plasmid (m) and VILL HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Vill homology arms to support homology-directed repair at defined Vill 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.