PT Double Nickase Plasmid (h): sc-417829-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PT 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
- PT Double Nickase Plasmid (h) and PT Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PTMA. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PT Double Nickase Plasmid (h) | sc-417829-NIC | 20 µg | $410.00 |
Human PTMA encodes prothymosin alpha, a small acidic nuclear protein implicated in chromatin organization, histone binding, and regulation of transcriptional programs linked to cell proliferation and survival. PTMA participates in processes such as apoptosis control, oxidative stress responses, and cell cycle progression, and has been connected to pathways involving NF-κB signaling and broader stress-induced gene expression networks. Dysregulated PTMA expression has been reported across multiple cancer contexts and immune-related settings, supporting its use as a mechanistic node in studies of tumor biology, inflammation, and cell fate regulation. As a predominantly nuclear factor, PTMA is also used to interrogate how chromatin-associated proteins influence genome stability and transcriptional plasticity.
PT Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PTMA locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PTMA. 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 PTMA 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 PTMA-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.