TRIM2 Double Nickase Plasmid (h): sc-410495-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRIM2 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
- TRIM2 Double Nickase Plasmid (h) and TRIM2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TRIM2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRIM2 Double Nickase Plasmid (h) | sc-410495-NIC | 20 µg | $410.00 | |||
TRIM2 Double Nickase Plasmid (h2) | sc-410495-NIC-2 | 20 µg | $410.00 |
TRIM2 encodes a tripartite motif–containing E3 ubiquitin ligase implicated in ubiquitin-dependent protein turnover and cytoskeletal organization, with prominent roles in neuronal maintenance. Through its RING, B-box, and coiled-coil domains, TRIM2 participates in proteostasis and stress-response pathways that shape axon integrity, synaptic function, and intracellular trafficking. Altered TRIM2 activity has been associated with neurodevelopmental and neurodegenerative phenotypes, consistent with its enrichment in the nervous system and involvement in regulating stability of key neuronal substrates. These properties make TRIM2 a useful node for studying ubiquitin–proteasome regulation, cytoskeletal dynamics, and cell type–specific vulnerability mechanisms.
TRIM2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TRIM2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TRIM2. 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 TRIM2 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 TRIM2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.