B7-H4 CRISPR/Cas9 KO Plasmid (h): sc-416865
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- B7-H4 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 B7-H4 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 | |
B7-H4 CRISPR/Cas9 KO Plasmid (h) | sc-416865 | 20 µg | $397.00 |
Overview
VTCN1 encodes B7-H4 (V-set domain containing T cell activation inhibitor 1), a B7 family immune checkpoint ligand that suppresses T cell proliferation and cytokine production, contributing to peripheral immune regulation. B7-H4 is induced in myeloid and epithelial contexts and influences antigen presentation, inflammatory signaling, and immune evasion programs within the tumor microenvironment. Dysregulated VTCN1 expression has been reported across multiple solid tumors and is associated with reduced antitumor immune activity, while also intersecting with pathways governing macrophage polarization and T cell activation thresholds. These attributes make VTCN1 a useful target for dissecting inhibitory co-signaling networks and immunoregulatory mechanisms relevant to cancer and chronic inflammation models.
B7-H4 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the VTCN1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the VTCN1 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 VTCN1 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 B7-H4 protein expression.
This CRISPR knockout system enables efficient generation of VTCN1-deficient cell models for investigation of B7-H4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting VTCN1 exon(s) critical for B7-H4 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 VTCN1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by B7-H4 CRISPR/Cas9 KO Plasmid (h) and B7-H4 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the VTCN1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by B7-H4 HDR Plasmid (h) and B7-H4 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by VTCN1 homology arms to support homology-directed repair at defined VTCN1 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.