NBK Double Nickase Plasmid (m): sc-419331-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NBK Double Nickase Plasmid (m) 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
- NBK Double Nickase Plasmid (m) and NBK Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Bik. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NBK Double Nickase Plasmid (m) | sc-419331-NIC | 20 µg | $410.00 | |||
NBK Double Nickase Plasmid (m2) | sc-419331-NIC-2 | 20 µg | $410.00 |
Bik encodes NBK, a BH3-only pro-apoptotic member of the BCL-2 family that promotes mitochondrial outer membrane permeabilization by neutralizing anti-apoptotic proteins such as BCL-2, BCL-XL, and MCL1. In mouse cells, NBK contributes to intrinsic apoptosis, endoplasmic reticulum stress–linked death signaling, and regulation of tissue homeostasis through caspase activation. BI K/NBK activity intersects with p53-associated stress responses and BCL-2–regulated checkpoints that influence cell survival decisions. Dysregulation of BCL-2 family balance, including altered Bik expression, is frequently studied in contexts such as oncogenic transformation, immune cell selection, and neurodegeneration models where apoptotic threshold is perturbed.
NBK Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Bik locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Bik. 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 Bik 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 Bik-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.