B7-H4 Double Nickase Plasmid (h): sc-416865-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- B7-H4 Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- B7-H4 Double Nickase Plasmid (h) and B7-H4 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting VTCN1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
B7-H4 Double Nickase Plasmid (h) | sc-416865-NIC | 20 µg | $410.00 |
VTCN1 encodes B7-H4 (V-set domain-containing T-cell activation inhibitor 1), an immune checkpoint molecule in the B7 family that suppresses T-cell proliferation and cytokine production, thereby shaping peripheral immune tolerance. B7-H4 is typically low in most normal tissues but can be induced on antigen-presenting cells and various epithelial contexts, linking its regulation to inflammatory cues and tumor–immune interactions. By modulating costimulatory signaling and downstream pathways that influence T-cell activation states, B7-H4 contributes to immune evasion mechanisms and is frequently studied in oncology and chronic inflammatory disease models. Altered VTCN1/B7-H4 expression is associated with changes in immune infiltration and immunosuppressive microenvironments, making it relevant for mechanistic studies of immune regulation.
B7-H4 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the VTCN1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within VTCN1. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt VTCN1 function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of VTCN1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.