PLUNC Double Nickase Plasmid (h): sc-416774-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PLUNC 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
- PLUNC Double Nickase Plasmid (h) and PLUNC Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting BPIFA1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: PLUNC Antibody (A-11): sc-271457
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PLUNC Double Nickase Plasmid (h) | sc-416774-NIC | 20 µg | $410.00 | |||
PLUNC Double Nickase Plasmid (h2) | sc-416774-NIC-2 | 20 µg | $410.00 |
BPIFA1 encodes the human PLUNC protein, a secreted member of the BPI fold-containing family that is enriched in upper airway and nasopharyngeal epithelium. PLUNC contributes to innate mucosal defense by modulating airway surface liquid homeostasis, influencing epithelial barrier function, and interacting with microbial components that shape local inflammatory signaling. BPIFA1 expression is responsive to epithelial differentiation and inflammatory cues, linking it to processes such as host–pathogen interactions, mucociliary clearance, and regulation of airway milieu. Altered BPIFA1/PLUNC abundance has been reported in respiratory inflammatory contexts and is frequently studied in relation to chronic airway disease mechanisms and epithelial remodeling.
PLUNC Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the BPIFA1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within BPIFA1. 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 BPIFA1 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 BPIFA1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.