VDAC2 Double Nickase Plasmid (h): sc-416966-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- VDAC2 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
- VDAC2 Double Nickase Plasmid (h) and VDAC2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting VDAC2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
VDAC2 Double Nickase Plasmid (h) | sc-416966-NIC | 20 µg | $410.00 | |||
VDAC2 Double Nickase Plasmid (h2) | sc-416966-NIC-2 | 20 µg | $410.00 |
VDAC2 encodes voltage-dependent anion channel 2, a β-barrel pore in the outer mitochondrial membrane that governs exchange of metabolites and ions between the cytosol and mitochondria. By shaping mitochondrial permeability and coordinating interactions with BCL-2 family proteins, VDAC2 influences apoptosis, mitochondrial dynamics, and cellular bioenergetics. It is linked to processes such as oxidative phosphorylation, redox homeostasis, and stress signaling at mitochondria-associated membranes. Dysregulation of VDAC2-dependent mitochondrial control has been investigated in contexts including altered cell death susceptibility, cardiometabolic stress, and cancer cell survival phenotypes.
VDAC2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the VDAC2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within VDAC2. 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 VDAC2 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 VDAC2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.