p53 Double Nickase Plasmid (r): sc-437318-NIC
- Target species: rat
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- p53 Double Nickase Plasmid (r) 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
- p53 Double Nickase Plasmid (r) and p53 Double Nickase Plasmid (r2) encode distinct paired gRNA designs targeting . One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
p53 Double Nickase Plasmid (r) | sc-437318-NIC | 20 µg | $410.00 | |||
p53 Double Nickase Plasmid (r2) | sc-437318-NIC-2 | 20 µg | $410.00 |
Rat p53 is a central tumor suppressor transcription factor that safeguards genomic integrity by coordinating DNA damage sensing with cell cycle arrest, senescence, and apoptosis. Following genotoxic stress, p53 integrates signals from ATM/ATR and CHK1/CHK2 pathways to modulate transcriptional programs controlling checkpoints, DNA repair, and mitochondrial apoptotic signaling. Its activity is tightly regulated by negative feedback with MDM2/MDM4 and shaped by post-translational modifications that tune stability and promoter selectivity. Disruption of p53-dependent surveillance is strongly linked to oncogenic transformation, altered stress tolerance, and dysregulated inflammatory and metabolic responses in disease-relevant models.
p53 Double Nickase Plasmid (r) consists of a matched pair of plasmids engineered for high-specificity editing of the locus in rat 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.