Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
L-type Ca++ CP α1C Double Nickase Plasmid (h): sc-401062-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- L-type Ca++ CP α1C 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
- L-type Ca++ CP α1C Double Nickase Plasmid (h) and L-type Ca++ CP α1C Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CACNA1C. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: L-type Ca++ CP α1C Antibody (D-6): sc-398433
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
L-type Ca++ CP α1C Double Nickase Plasmid (h) | sc-401062-NIC | 20 µg | $410.00 | |||
L-type Ca++ CP α1C Double Nickase Plasmid (h2) | sc-401062-NIC-2 | 20 µg | $410.00 |
CACNA1C encodes the α1C pore-forming subunit (CaV1.2) of L-type voltage-gated Ca2+ channels that mediate depolarization-evoked Ca2+ influx in excitable and non-excitable cells. CaV1.2-driven calcium entry couples membrane activity to intracellular signaling, including excitation–contraction coupling, synaptic integration, and calcium-dependent transcription via pathways such as CaM/CaMK and calcineurin–NFAT. Channel activity influences cardiac and smooth muscle electrophysiology as well as neuronal plasticity by shaping action potential dynamics and downstream gene expression programs. Genetic variation or dysregulation of CACNA1C is associated with cardiovascular phenotypes and neuropsychiatric disease risk, making it a widely studied node in calcium signaling networks.
L-type Ca++ CP α1C Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CACNA1C locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CACNA1C. 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 CACNA1C 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 CACNA1C-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.