CAMP Double Nickase Plasmid (h): sc-400651-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CAMP 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
- CAMP Double Nickase Plasmid (h) and CAMP Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CAMP. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: LL-37 Antibody (D-5): sc-166770
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CAMP Double Nickase Plasmid (h) | sc-400651-NIC | 20 µg | $410.00 | |||
CAMP Double Nickase Plasmid (h2) | sc-400651-NIC-2 | 20 µg | $410.00 |
Human CAMP encodes cathelicidin antimicrobial peptide (LL-37), a cationic host-defense effector produced by epithelial cells and myeloid lineages. CAMP contributes to innate immune pathways by directly disrupting microbial membranes and by modulating pattern-recognition receptor signaling, chemotaxis, and cytokine responses during inflammation. Beyond antimicrobial activity, LL-37 influences epithelial barrier homeostasis, wound repair programs, and leukocyte recruitment in mucosal tissues. Dysregulated CAMP expression has been linked to inflammatory skin and airway conditions, altered susceptibility to infection, and tumor-associated immune remodeling, making it a useful node for studying immunometabolic and microenvironmental signaling.
CAMP Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CAMP locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CAMP. 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 CAMP 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 CAMP-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.