Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
BID Double Nickase Plasmid (m): sc-419329-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BID 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
- BID Double Nickase Plasmid (m) and BID Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Bid. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: BID Antibody (F-5): sc-515616
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BID Double Nickase Plasmid (m) | sc-419329-NIC | 20 µg | $410.00 | |||
BID Double Nickase Plasmid (m2) | sc-419329-NIC-2 | 20 µg | $410.00 |
Mouse Bid encodes BID, a BH3-only BCL-2 family protein that couples extrinsic death receptor signaling to the mitochondrial apoptotic pathway. Following proteolytic cleavage to truncated BID (tBID), it promotes BAX/BAK-mediated mitochondrial outer membrane permeabilization, cytochrome c release, and caspase cascade activation, integrating crosstalk between apoptosis and cellular stress responses. BID activity is linked to regulation of immune homeostasis, hepatocyte survival, and inflammatory signaling through TNF/Fas pathways, and its dysregulation is implicated in mechanisms relevant to oncogenesis and tissue injury models. As a nodal apoptotic regulator, BID is commonly studied in contexts such as DNA damage responses, mitochondrial dynamics, and cell fate decisions under cytokine or genotoxic stress.
BID Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Bid locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Bid. 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 Bid 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 Bid-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.