CLIC2 Double Nickase Plasmid (h): sc-409129-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CLIC2 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
- CLIC2 Double Nickase Plasmid (h) and CLIC2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CLIC2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CLIC2 Double Nickase Plasmid (h) | sc-409129-NIC | 20 µg | $410.00 | |||
CLIC2 Double Nickase Plasmid (h2) | sc-409129-NIC-2 | 20 µg | $410.00 |
CLIC2 encodes chloride intracellular channel protein 2, a member of the CLIC family implicated in ion homeostasis and redox-sensitive regulation of intracellular membranes. CLIC2 is associated with processes such as endosomal trafficking, cytoskeletal dynamics, and modulation of calcium-dependent signaling through interactions with ryanodine receptors in excitable cells. Altered CLIC2 expression or function has been linked to neurodevelopmental and cardiovascular phenotypes, supporting its relevance in studies of neuronal excitability, muscle physiology, and stress-responsive signaling. In human cell models, CLIC2 perturbation can be used to probe how intracellular chloride flux and channel-associated scaffolding affect membrane potential, vesicle biology, and oxidative stress responses.
CLIC2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CLIC2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CLIC2. 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 CLIC2 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 CLIC2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.