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 α1D Double Nickase Plasmid (h): sc-401745-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- L-type Ca++ CP α1D 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 α1D Double Nickase Plasmid (h) and L-type Ca++ CP α1D Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CACNA1D. 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 α1D Antibody (E-3): sc-515679
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
L-type Ca++ CP α1D Double Nickase Plasmid (h) | sc-401745-NIC | 20 µg | $410.00 | |||
L-type Ca++ CP α1D Double Nickase Plasmid (h2) | sc-401745-NIC-2 | 20 µg | $410.00 |
CACNA1D encodes the α1D pore-forming subunit of L-type voltage-gated calcium channels (CaV1.3), which mediate membrane depolarization–evoked Ca2+ influx and shape excitation–transcription coupling. CaV1.3-dependent calcium entry regulates neuronal firing patterns, hormone secretion, and activity-dependent gene expression through Ca2+/calmodulin signaling and downstream pathways such as CaMK and calcineurin/NFAT. In excitable tissues, CACNA1D contributes to pacemaking behavior and calcium-dependent synaptic and transcriptional plasticity. Dysregulation or genetic variation in CACNA1D has been linked to neurodevelopmental and neuropsychiatric phenotypes as well as endocrine and cardiovascular physiology, supporting its relevance in ion channel biology and disease mechanism studies.
L-type Ca++ CP α1D Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CACNA1D locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CACNA1D. 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 CACNA1D 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 CACNA1D-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.