PDE3A Double Nickase Plasmid (h): sc-402183-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PDE3A 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
- PDE3A Double Nickase Plasmid (h) and PDE3A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PDE3A. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: PDE3A Antibody (2D7): sc-293446
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PDE3A Double Nickase Plasmid (h) | sc-402183-NIC | 20 µg | $410.00 | |||
PDE3A Double Nickase Plasmid (h2) | sc-402183-NIC-2 | 20 µg | $410.00 |
Phosphodiesterase 3A (PDE3A) is a dual-specificity cyclic nucleotide phosphodiesterase that hydrolyzes cAMP and cGMP, thereby shaping second-messenger dynamics downstream of GPCR and nitric oxide signaling. By controlling cyclic nucleotide turnover, PDE3A influences PKA/PKG-regulated processes including ion channel activity, platelet function, and vascular smooth muscle contractility, as well as broader signal integration between cAMP and cGMP pathways. Altered PDE3A activity has been associated with dysregulated cardiovascular and hematologic phenotypes, making it a useful target for mechanistic studies of cyclic nucleotide–dependent signaling networks in human cells.
PDE3A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PDE3A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PDE3A. 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 PDE3A 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 PDE3A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.