TRAF6 Double Nickase Plasmid (m): sc-423497-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRAF6 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
- TRAF6 Double Nickase Plasmid (m) and TRAF6 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Traf6. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TRAF6 Antibody (D-10): sc-8409
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRAF6 Double Nickase Plasmid (m) | sc-423497-NIC | 20 µg | $410.00 | |||
TRAF6 Double Nickase Plasmid (m2) | sc-423497-NIC-2 | 20 µg | $410.00 |
Mouse Traf6 encodes the E3 ubiquitin ligase TRAF6, an adaptor that couples upstream receptors to downstream signaling in innate and adaptive immunity. TRAF6 mediates K63-linked ubiquitination events that drive activation of NF-κB and MAPK cascades downstream of Toll-like receptors, IL-1 receptor family members, CD40, and RANK, shaping cytokine production, osteoclast differentiation, and inflammatory gene expression programs. Through these pathways, TRAF6 influences host defense, tissue remodeling, and immune homeostasis, and its dysregulation is studied in contexts such as chronic inflammation, bone metabolism disorders, and immune-mediated pathologies.
TRAF6 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Traf6 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Traf6. 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 Traf6 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 Traf6-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.