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.
MaxiKα Double Nickase Plasmid (h): sc-402208-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MaxiKα 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
- MaxiKα Double Nickase Plasmid (h) and MaxiKα Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KCNMA1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MaxiKα Antibody (B-1): sc-374142
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MaxiKα Double Nickase Plasmid (h) | sc-402208-NIC | 20 µg | $410.00 | |||
MaxiKα Double Nickase Plasmid (h2) | sc-402208-NIC-2 | 20 µg | $410.00 |
KCNMA1 encodes the human MaxiKα (BK, KCa1.1) large-conductance, voltage- and Ca2+-activated potassium channel α subunit, a central regulator of membrane excitability and intracellular calcium signaling. By coupling elevations in cytosolic Ca2+ and depolarization to K+ efflux, MaxiKα shapes action potential repolarization, neurotransmitter release, smooth muscle tone, and mechanotransduction across many cell types. Channel function is integrated with GPCR and kinase signaling pathways, and is strongly modulated by auxiliary β/γ subunits and local Ca2+ microdomains. Dysregulated KCNMA1 activity or altered channel gating has been linked to neurological phenotypes, including epilepsy and movement disorders, and to functional changes in vascular and airway physiology relevant to cardiopulmonary research.
MaxiKα Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KCNMA1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KCNMA1. 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 KCNMA1 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 KCNMA1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.