HCN2 Double Nickase Plasmid (h): sc-405074-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HCN2 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
- HCN2 Double Nickase Plasmid (h) and HCN2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HCN2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HCN2 Double Nickase Plasmid (h) | sc-405074-NIC | 20 µg | $410.00 | |||
HCN2 Double Nickase Plasmid (h2) | sc-405074-NIC-2 | 20 µg | $410.00 |
HCN2 encodes the hyperpolarization-activated cyclic nucleotide–gated channel 2, a membrane ion channel that carries the Ih/If current and contributes to pacemaker activity and rhythmic excitability in neurons and cardiac conduction tissues. Channel opening is triggered by membrane hyperpolarization and is modulated by intracellular cAMP, linking HCN2 to GPCR–adenylyl cyclase signaling and activity-dependent control of membrane potential. By shaping resting potential, input resistance, and rebound firing, HCN2 influences synaptic integration and network oscillations in excitable cells. Altered HCN2 function or expression has been associated with disorders of excitability, including epilepsy and neuropathic pain phenotypes, supporting its utility as a mechanistic target in ion-channel and neurophysiology research.
HCN2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HCN2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HCN2. 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 HCN2 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 HCN2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.