CaM II Double Nickase Plasmid (h): sc-400952-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CaM II 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
- CaM II Double Nickase Plasmid (h) and CaM II Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CALM2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CaM II Double Nickase Plasmid (h) | sc-400952-NIC | 20 µg | $410.00 | |||
CaM II Double Nickase Plasmid (h2) | sc-400952-NIC-2 | 20 µg | $410.00 |
Human CALM2 encodes calmodulin (CaM II), a ubiquitously expressed Ca2+ sensor that translates transient calcium signals into coordinated changes in enzyme activity, ion channel gating, and transcriptional programs. By binding and regulating targets such as CaMKs, calcineurin, phosphodiesterases, and nitric oxide synthases, CALM2 contributes to excitation–contraction coupling, synaptic plasticity, vesicle trafficking, and cell-cycle control. CALM2-dependent signaling interfaces with Ca2+/calmodulin kinase pathways, MAPK cascades, and cytoskeletal remodeling to shape stimulus-dependent cellular responses. Dysregulated calmodulin signaling and calmodulin gene variants are linked to abnormal electrical excitability and altered Ca2+ homeostasis, motivating mechanistic studies in cardiomyocytes, neurons, and other excitable cell models.
CaM II Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CALM2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CALM2. 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 CALM2 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 CALM2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.