CaM III Double Nickase Plasmid (h): sc-400953-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CaM III 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 III Double Nickase Plasmid (h) and CaM III Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CALM3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CaM III Double Nickase Plasmid (h) | sc-400953-NIC | 20 µg | $410.00 | |||
CaM III Double Nickase Plasmid (h2) | sc-400953-NIC-2 | 20 µg | $410.00 |
Human CALM3 encodes calmodulin III (CaM III), a ubiquitously expressed Ca2+ sensor that binds diverse targets to convert transient calcium signals into coordinated cellular responses. CaM III regulates key processes including CaMK and calcineurin/NFAT signaling, cyclic nucleotide metabolism, and ion channel gating, thereby influencing excitation–contraction coupling, synaptic activity, secretion, and cell-cycle progression. Through modulation of phosphorylation and transcriptional programs, calmodulin-dependent pathways shape mitochondrial function and stress responses and are frequently interrogated in studies of arrhythmogenesis, neurodevelopmental phenotypes, and proliferative signaling. Altered calcium handling and calmodulin network dysfunction are therefore relevant to mechanistic models of cardiovascular and neurological disease and to pathway mapping in diverse cell types.
CaM III Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CALM3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CALM3. 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 CALM3 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 CALM3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.