TRIM69 Double Nickase Plasmid (h): sc-404906-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRIM69 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
- TRIM69 Double Nickase Plasmid (h) and TRIM69 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TRIM69. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRIM69 Double Nickase Plasmid (h) | sc-404906-NIC | 20 µg | $410.00 | |||
TRIM69 Double Nickase Plasmid (h2) | sc-404906-NIC-2 | 20 µg | $410.00 |
TRIM69 encodes a tripartite motif (TRIM) family E3 ubiquitin ligase implicated in ubiquitin-dependent regulation of protein stability and signaling. As a RING-B-box-coiled-coil protein, TRIM69 is linked to innate immune control of antiviral responses and modulation of interferon-associated pathways, influencing the turnover or activity of key signaling intermediates. Altered TRIM family ubiquitination programs can reshape inflammatory signaling, stress responses, and cell-state transitions, making TRIM69 relevant for mechanistic studies of immune regulation and host–pathogen interactions. Dysregulation of TRIM69-associated ubiquitin circuitry has also been explored in contexts where aberrant proteostasis and immune signaling contribute to disease phenotypes.
TRIM69 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TRIM69 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TRIM69. 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 TRIM69 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 TRIM69-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.