CDD Double Nickase Plasmid (h): sc-403915-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CDD 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
- CDD Double Nickase Plasmid (h) and CDD Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CDA. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CDD Antibody (D-5): sc-365292
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CDD Double Nickase Plasmid (h) | sc-403915-NIC | 20 µg | $410.00 | |||
CDD Double Nickase Plasmid (h2) | sc-403915-NIC-2 | 20 µg | $410.00 |
Human CDA encodes cytidine deaminase (CDD), a zinc-dependent enzyme that catalyzes deamination of cytidine and deoxycytidine to uridine and deoxyuridine, respectively. This activity contributes to pyrimidine salvage and nucleotide pool homeostasis, influencing DNA replication fidelity and cellular responses to nucleoside availability. CDA expression and enzymatic activity modulate intracellular levels of cytidine analog substrates and participate in metabolic networks linked to nucleoside transport and phosphorylation. Altered CDA function or expression has been associated with variability in nucleoside metabolism in cancer biology and hematologic contexts, making it relevant for mechanistic studies of metabolic adaptation and genotoxic stress.
CDD Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CDA locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CDA. 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 CDA 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 CDA-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.