TorsinA Double Nickase Plasmid (h): sc-404651-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TorsinA 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
- TorsinA Double Nickase Plasmid (h) and TorsinA Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TOR1A. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TorsinA Antibody (D-7): sc-373915
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TorsinA Double Nickase Plasmid (h) | sc-404651-NIC | 20 µg | $410.00 | |||
TorsinA Double Nickase Plasmid (h2) | sc-404651-NIC-2 | 20 µg | $410.00 |
TOR1A encodes TorsinA, an AAA+ ATPase that localizes to the endoplasmic reticulum and perinuclear space where it supports nuclear envelope integrity and endomembrane homeostasis. TorsinA participates in processes including nuclear pore complex biogenesis, membrane remodeling, and regulation of protein quality control pathways linked to ER stress. Disruption of TOR1A-associated functions can perturb nucleo-cytoskeletal coupling and intracellular trafficking, making it a key node for studying proteostasis and nuclear envelope–linked cellular phenotypes. Variants in TOR1A are strongly associated with early-onset dystonia and related neurobiology, providing a molecular entry point for mechanistic studies in neuronal and non-neuronal models.
TorsinA Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TOR1A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TOR1A. 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 TOR1A 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 TOR1A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.