TRAF7 Double Nickase Plasmid (h): sc-404992-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRAF7 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
- TRAF7 Double Nickase Plasmid (h) and TRAF7 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TRAF7. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRAF7 Double Nickase Plasmid (h) | sc-404992-NIC | 20 µg | $410.00 | |||
TRAF7 Double Nickase Plasmid (h2) | sc-404992-NIC-2 | 20 µg | $410.00 |
Human TRAF7 encodes an E3 ubiquitin ligase of the TRAF family that scaffolds and ubiquitinates signaling intermediates to modulate inflammatory and stress-responsive pathways. Through interactions with MAPK components and NF-κB–associated regulators, TRAF7 helps coordinate proteostasis, transcriptional responses, and cell fate decisions, including apoptosis under specific contexts. TRAF7 has been implicated in the control of ubiquitin-dependent signaling outputs and cross-talk with pathways governing cytoskeletal organization and cellular homeostasis. Recurrent TRAF7 alterations have been reported in several tumor types, supporting its relevance for studying ubiquitin signaling dysregulation in disease-associated cellular states.
TRAF7 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TRAF7 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TRAF7. 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 TRAF7 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 TRAF7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.