CALML3 Double Nickase Plasmid (h): sc-400954-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CALML3 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
- CALML3 Double Nickase Plasmid (h) and CALML3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CALML3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CALML3 Double Nickase Plasmid (h) | sc-400954-NIC | 20 µg | $410.00 | |||
CALML3 Double Nickase Plasmid (h2) | sc-400954-NIC-2 | 20 µg | $410.00 |
CALML3 (calmodulin-like 3) encodes a Ca2+-binding EF-hand protein that functions as a calcium sensor and modulator of calmodulin-dependent signaling. It is enriched in epithelial lineages and has been linked to cytoskeletal remodeling, cell–cell junction organization, and calcium-regulated phosphorylation networks that influence proliferation and differentiation. CALML3 activity intersects with pathways controlling keratinocyte maturation and epithelial homeostasis through regulation of Ca2+-dependent enzymes and scaffolding complexes. Dysregulated expression has been reported in multiple epithelial pathologies, including cancers, making CALML3 a useful target for studying how calcium signaling rewires adhesion and growth programs.
CALML3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CALML3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CALML3. 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 CALML3 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 CALML3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.