DR5 Double Nickase Plasmid (m): sc-423438-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DR5 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
- DR5 Double Nickase Plasmid (m) and DR5 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Tnfrsf10b. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: DR5 Antibody (7F4-F8-G11): sc-517559
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DR5 Double Nickase Plasmid (m) | sc-423438-NIC | 20 µg | $410.00 |
Mouse Tnfrsf10b encodes death receptor 5 (DR5), a TNF receptor superfamily member that binds TRAIL and initiates extrinsic apoptosis through receptor trimerization, FADD recruitment, and caspase-8 activation. DR5 signaling can intersect with mitochondrial amplification via BID and caspase-9, while also engaging NF-κB and MAPK pathways that influence inflammatory gene expression and stress responses. Regulation of DR5 expression and trafficking shapes sensitivity to death receptor signaling and contributes to cell fate decisions during immune surveillance and tissue homeostasis. Altered DR5 pathway activity is frequently studied in the context of tumor biology, immune regulation, and resistance to apoptotic cues in disease models.
DR5 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Tnfrsf10b locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Tnfrsf10b. 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 Tnfrsf10b 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 Tnfrsf10b-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.