TRPS1 Double Nickase Plasmid (h): sc-403037-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRPS1 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
- TRPS1 Double Nickase Plasmid (h) and TRPS1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TRPS1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRPS1 Double Nickase Plasmid (h) | sc-403037-NIC | 20 µg | $410.00 |
TRPS1 encodes a GATA-type zinc finger transcription factor that functions primarily as a transcriptional repressor during development, integrating signals that shape epithelial differentiation and skeletal patterning. TRPS1 regulates gene programs involved in chondrocyte maturation, hair follicle morphogenesis, and cell-cycle control through context-dependent interactions with chromatin remodeling and corepressor complexes. In human biology, altered TRPS1 expression or function is associated with tricho-rhino-phalangeal syndromes and has been linked to dysregulated transcriptional networks in hormone-responsive epithelial tissues, making it relevant for studies of lineage specification and transcriptional control. As a nuclear DNA-binding protein, TRPS1 is frequently investigated in pathways governing differentiation, proliferation, and tissue-specific gene expression.
TRPS1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TRPS1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TRPS1. 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 TRPS1 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 TRPS1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.