D54 Double Nickase Plasmid (h): sc-407162-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- D54 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
- D54 Double Nickase Plasmid (h) and D54 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TPD52L2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
D54 Double Nickase Plasmid (h) | sc-407162-NIC | 20 µg | $410.00 | |||
D54 Double Nickase Plasmid (h2) | sc-407162-NIC-2 | 20 µg | $410.00 |
TPD52L2 encodes D54, a cytosolic coiled-coil protein in the tumor protein D52 family that associates with membrane trafficking compartments and is implicated in regulation of vesicle transport, exocytosis, and endomembrane dynamics. D54 has been linked to proliferative signaling and cellular metabolic adaptation, with reported connections to pathways influencing cell cycle progression and stress responses. Altered TPD52L2 expression has been observed across multiple tumor contexts, supporting its use as a research target for studying oncogenic growth programs, migration, and organelle remodeling. In cell models, perturbation of D54 provides a route to dissect how trafficking-associated scaffolds coordinate signaling outputs and proteostasis.
D54 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TPD52L2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TPD52L2. 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 TPD52L2 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 TPD52L2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.