TRP2/DCT Double Nickase Plasmid (h): sc-400334-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRP2/DCT 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
- TRP2/DCT Double Nickase Plasmid (h) and TRP2/DCT Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DCT. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TRP2/DCT Antibody (C-9): sc-74439
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRP2/DCT Double Nickase Plasmid (h) | sc-400334-NIC | 20 µg | $410.00 | |||
TRP2/DCT Double Nickase Plasmid (h2) | sc-400334-NIC-2 | 20 µg | $410.00 |
Human DCT (dopachrome tautomerase), also known as TRP2, is a melanosomal enzyme in the eumelanin biosynthetic pathway that catalyzes dopachrome conversion to DHICA, shaping pigment composition and redox balance in melanocytes. Its expression is regulated by melanocyte lineage programs such as MITF-dependent transcription and integrates with melanosome biogenesis and trafficking processes. DCT activity influences cellular responses to oxidative stress and differentiation states, making it relevant to studies of pigmentation biology and melanocyte function. Dysregulated DCT expression is frequently examined in melanoma and other pigment cell–associated disorders as a marker of lineage identity and tumor biology.
TRP2/DCT Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DCT locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DCT. 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 DCT 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 DCT-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.