Bax Double Nickase Plasmid (h): sc-400042-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Bax 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
- Bax Double Nickase Plasmid (h) and Bax Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting BAX. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Bax Antibody (B-9): sc-7480
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Bax Double Nickase Plasmid (h) | sc-400042-NIC | 20 µg | $410.00 | |||
Bax Double Nickase Plasmid (h2) | sc-400042-NIC-2 | 20 µg | $410.00 |
BAX encodes Bax, a pro-apoptotic BCL-2 family effector that governs mitochondrial outer membrane permeabilization and commits cells to intrinsic apoptosis. In response to cellular stress and DNA damage signals, Bax undergoes conformational activation, translocates to mitochondria, and oligomerizes to promote cytochrome c release and downstream caspase activation. Bax activity integrates with p53-regulated checkpoints and survival signaling networks, thereby shaping cell fate decisions during development and tissue homeostasis. Dysregulated BAX signaling is broadly implicated in cancer biology, neurodegeneration, and responses to genotoxic stress, making it a widely used node for studying apoptosis and mitochondrial pathway control.
Bax Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the BAX locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within BAX. 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 BAX 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 BAX-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.