p53 Double Nickase Plasmid (h): sc-416469-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- p53 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
- p53 Double Nickase Plasmid (h) and p53 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TP53. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: p53 Antibody (DO-1): sc-126
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
p53 Double Nickase Plasmid (h) | sc-416469-NIC | 20 µg | $410.00 | |||
p53 Double Nickase Plasmid (h2) | sc-416469-NIC-2 | 20 µg | $410.00 |
TP53 encodes the human p53 tumor suppressor, a sequence-specific transcription factor that integrates cellular stress signals to coordinate DNA damage responses, cell-cycle arrest, senescence, and apoptosis. p53 activity is regulated by post-translational modifications and feedback control through the MDM2 axis, and it modulates pathways including G1/S and G2/M checkpoints, homologous recombination, and nucleotide excision repair. Disruption of TP53 function alters genomic stability, cell fate decisions, and transcriptional programs linked to oncogenic transformation. TP53 is among the most frequently altered genes in human cancers, making p53 a central node for studying stress signaling, genome maintenance, and tumor biology.
p53 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TP53 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TP53. 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 TP53 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 TP53-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.