GDPD3 Double Nickase Plasmid (h): sc-405288-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GDPD3 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
- GDPD3 Double Nickase Plasmid (h) and GDPD3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GDPD3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GDPD3 Double Nickase Plasmid (h) | sc-405288-NIC | 20 µg | $410.00 | |||
GDPD3 Double Nickase Plasmid (h2) | sc-405288-NIC-2 | 20 µg | $410.00 |
GDPD3 (glycerophosphodiester phosphodiesterase domain containing 3) encodes a putative glycerophosphodiester phosphodiesterase implicated in phospholipid and glycerophosphocholine metabolism, linking membrane lipid remodeling to cellular signaling output. By influencing levels of lysophospholipids and related metabolites, GDPD3 is positioned to modulate pathways connected to membrane dynamics, lipid second messengers, and metabolic adaptation. Altered lipid metabolic programs are frequently observed in proliferative and stress-response states, making GDPD3 a useful node for studying lipid-driven regulation of growth, survival, and inflammation-associated signaling. Dysregulation of phospholipid turnover has been associated with cancer and metabolic disease phenotypes, supporting investigation of GDPD3 in disease-relevant cell models.
GDPD3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GDPD3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GDPD3. 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 GDPD3 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 GDPD3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.