ΔN p73 Double Nickase Plasmid (h): sc-437274-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ΔN p73 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
- ΔN p73 Double Nickase Plasmid (h) and ΔN p73 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting . One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ΔN p73 Double Nickase Plasmid (h) | sc-437274-NIC | 20 µg | $410.00 | |||
ΔN p73 Double Nickase Plasmid (h2) | sc-437274-NIC-2 | 20 µg | $410.00 |
ΔN p73 is an N-terminally truncated isoform of human TP73 that lacks the canonical transactivation domain and can act as a dominant-negative regulator of p53 family transcriptional programs. By modulating DNA damage responses, apoptosis, and cell-cycle control, ΔN p73 influences stress signaling networks that intersect with p53/p63-dependent gene regulation. Altered ΔN p73 expression has been associated with tumorigenesis and therapy resistance phenotypes in multiple cancer contexts through disruption of pro-apoptotic and checkpoint pathways. Its activity is also relevant to differentiation and survival decisions in epithelial and neural lineages, making it a useful node for studying isoform-specific transcriptional control.
ΔN p73 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within . 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 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 -disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.