TRIM31 Double Nickase Plasmid (h): sc-411560-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRIM31 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
- TRIM31 Double Nickase Plasmid (h) and TRIM31 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TRIM31. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRIM31 Double Nickase Plasmid (h) | sc-411560-NIC | 20 µg | $410.00 | |||
TRIM31 Double Nickase Plasmid (h2) | sc-411560-NIC-2 | 20 µg | $410.00 |
TRIM31 encodes tripartite motif-containing protein 31, a RING-type E3 ubiquitin ligase that participates in ubiquitin-dependent protein turnover and innate immune regulation. Through TRIM family signaling, TRIM31 has been linked to control of antiviral responses, modulation of NF-κB and related inflammatory pathways, and regulation of protein homeostasis via proteasome-directed ubiquitination. Altered TRIM31 activity can perturb immune signaling, stress responses, and cellular growth control, making it relevant to studies of inflammation-associated phenotypes and tumor biology. As a cytoplasmic regulator of ubiquitin signaling, TRIM31 is frequently investigated for its effects on pathway tuning and stimulus-dependent transcriptional outputs.
TRIM31 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TRIM31 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TRIM31. 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 TRIM31 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 TRIM31-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.