CLEC-9A Double Nickase Plasmid (m): sc-433169-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CLEC-9A Double Nickase Plasmid (m) 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
- CLEC-9A Double Nickase Plasmid (m) and CLEC-9A Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Clec9a. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CLEC-9A Double Nickase Plasmid (m) | sc-433169-NIC | 20 µg | $410.00 |
Mouse Clec9a encodes CLEC-9A (DNGR-1), a C-type lectin receptor selectively expressed by conventional dendritic cell subsets that specialize in sensing cell damage. CLEC-9A binds exposed actin structures from necrotic cells and promotes uptake and cross-presentation of dead-cell–associated antigens, shaping CD8+ T cell priming. Signaling is coupled to a hemITAM motif and Syk-dependent pathways that influence antigen processing, phagosomal maturation, and inflammatory programming in dendritic cells. Altered CLEC-9A function is relevant to studies of sterile inflammation, tumor antigen cross-priming, antiviral immunity, and autoimmune pathogenesis where dendritic cell handling of dying cells can modulate immune activation.
CLEC-9A Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Clec9a locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Clec9a. 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 Clec9a 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 Clec9a-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.