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.
MaxiKβ Double Nickase Plasmid (h): sc-403096-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MaxiKβ 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
- MaxiKβ Double Nickase Plasmid (h) and MaxiKβ Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KCNMB1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MaxiKβ Antibody (A-5): sc-377023
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MaxiKβ Double Nickase Plasmid (h) | sc-403096-NIC | 20 µg | $410.00 | |||
MaxiKβ Double Nickase Plasmid (h2) | sc-403096-NIC-2 | 20 µg | $410.00 |
KCNMB1 encodes the β1 regulatory subunit of the large-conductance, calcium- and voltage-activated potassium (BK/MaxiK) channel, which tunes channel gating by increasing apparent Ca²⁺ sensitivity and shaping membrane repolarization. In human smooth muscle and other excitable tissues, MaxiKβ1 couples intracellular Ca²⁺ signals to potassium efflux, influencing vascular tone, airway contractility, and neuronal firing through feedback regulation of membrane potential. This modulatory role links KCNMB1 to Ca²⁺-dependent signaling, electromechanical coupling, and nitric oxide/cGMP-responsive pathways that converge on ion channel control. Altered BK channel β1 function has been investigated in the context of blood pressure regulation, smooth muscle hyperreactivity, and disorders of excitability, making KCNMB1 a useful target for mechanistic ion channel research.
MaxiKβ Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KCNMB1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KCNMB1. 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 KCNMB1 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 KCNMB1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.