TRAF2 Double Nickase Plasmid (h): sc-400361-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRAF2 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
- TRAF2 Double Nickase Plasmid (h) and TRAF2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TRAF2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TRAF2 Antibody (F-2): sc-136999
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRAF2 Double Nickase Plasmid (h) | sc-400361-NIC | 20 µg | $410.00 | |||
TRAF2 Double Nickase Plasmid (h2) | sc-400361-NIC-2 | 20 µg | $410.00 |
TRAF2 (TNF receptor–associated factor 2) is an adaptor and E3 ubiquitin ligase that couples TNF receptor superfamily signaling to downstream transcriptional and stress-response pathways. Through interactions with TRAF-binding motifs and regulation of K63-linked ubiquitination, TRAF2 helps coordinate activation of NF-κB and MAPK cascades, shaping cytokine responses, apoptosis resistance, and cellular homeostasis. Its activity interfaces with RIPK1-dependent signaling complexes and influences cross-talk between inflammatory signaling and cell death programs. Dysregulated TRAF2 signaling has been implicated in altered immune regulation and oncogenic pathway remodeling, making it a useful node for mechanistic studies of inflammation-associated phenotypes.
TRAF2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TRAF2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TRAF2. 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 TRAF2 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 TRAF2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.