CDIP Double Nickase Plasmid (h): sc-409425-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CDIP 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
- CDIP Double Nickase Plasmid (h) and CDIP Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CDIP1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CDIP Double Nickase Plasmid (h) | sc-409425-NIC | 20 µg | $410.00 | |||
CDIP Double Nickase Plasmid (h2) | sc-409425-NIC-2 | 20 µg | $410.00 |
CDIP1 encodes CDIP, a stress-responsive protein originally identified as a p53 target that contributes to apoptotic signaling and cell fate decisions under genotoxic and oxidative stress. CDIP has been linked to mitochondrial pathways of apoptosis and modulation of DNA damage responses, intersecting with p53-regulated transcriptional programs and downstream caspase activation. Altered CDIP1/CDIP activity has been associated with dysregulated survival signaling in cancer-related contexts, including impacts on tumor cell sensitivity to stress and chemotherapy-associated damage. These properties make CDIP1 a useful node for studying mechanisms of apoptosis, stress adaptation, and p53 pathway rewiring in human cells.
CDIP Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CDIP1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CDIP1. 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 CDIP1 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 CDIP1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.