



Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRAF3 Double Nickase Plasmid (h) | sc-400473-NIC | 20 µg | $410.00 | |||
TRAF3 Double Nickase Plasmid (h2) | sc-400473-NIC-2 | 20 µg | $410.00 |
TRAF3 (TNF receptor–associated factor 3) is an adaptor and E3 ubiquitin ligase that coordinates signaling downstream of TNF receptor superfamily members, Toll-like receptors, and select pattern-recognition receptors. By regulating ubiquitin-dependent assembly of signaling complexes, TRAF3 shapes type I interferon responses, MAPK activity, and NF-κB pathway output, including restraint of noncanonical NF-κB signaling through control of NIK stability. These functions position TRAF3 as a key determinant of innate and adaptive immune homeostasis, influencing cytokine production, antigen receptor signaling, and cell survival decisions. Altered TRAF3 expression or function is linked to immune dysregulation and has been reported in malignancy-associated signaling contexts, supporting its use as a mechanistic node in inflammation and cancer biology research.
TRAF3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TRAF3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TRAF3. 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 TRAF3 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 TRAF3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.