Trio Double Nickase Plasmid (h): sc-401231-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Trio 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
- Trio Double Nickase Plasmid (h) and Trio Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TRIO. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Trio Double Nickase Plasmid (h) | sc-401231-NIC | 20 µg | $410.00 | |||
Trio Double Nickase Plasmid (h2) | sc-401231-NIC-2 | 20 µg | $410.00 |
Human TRIO encodes Trio, a multidomain Rho guanine nucleotide exchange factor that activates Rho-family GTPases, including RAC1 and RHOA, to coordinate actin cytoskeleton remodeling, cell polarity, migration, and neurite outgrowth. Trio integrates signals from membrane receptors and adhesion complexes into pathways controlling lamellipodia formation, axon guidance, and synaptic development. Through these roles, TRIO contributes to regulated tissue morphogenesis and nervous system connectivity, and its dysregulation has been associated with altered cytoskeletal dynamics in cancer biology and with neurodevelopmental disorders affecting neuronal wiring.
Trio Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TRIO locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TRIO. 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 TRIO 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 TRIO-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.