Tctex1 Double Nickase Plasmid (m): sc-423318-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Tctex1 Double Nickase Plasmid (m) 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
- Tctex1 Double Nickase Plasmid (m) and Tctex1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Dynlt1b. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Tctex1 Double Nickase Plasmid (m) | sc-423318-NIC | 20 µg | $410.00 | |||
Tctex1 Double Nickase Plasmid (m2) | sc-423318-NIC-2 | 20 µg | $410.00 |
Dynlt1b encodes the mouse Tctex1 light chain of cytoplasmic dynein, a microtubule-based motor complex that drives retrograde transport, organelle positioning, and mitotic spindle functions. Tctex1 contributes to dynein-dependent trafficking of vesicles and protein complexes, supporting processes such as intracellular signaling, neuronal transport, and ciliogenesis through coordinated microtubule dynamics. Perturbation of dynein light-chain interactions can disrupt cargo binding and transport fidelity, linking dynein pathway dysfunction to phenotypes relevant to neurodevelopment, ciliary biology, and cell division control. As a result, Dynlt1b is frequently studied in the context of cytoskeletal regulation, centrosome/spindle organization, and transport-dependent signaling pathways.
Tctex1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Dynlt1b locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Dynlt1b. 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 Dynlt1b 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 Dynlt1b-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.