ABHD7 Double Nickase Plasmid (h): sc-408425-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ABHD7 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
- ABHD7 Double Nickase Plasmid (h) and ABHD7 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting EPHX4. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ABHD7 Double Nickase Plasmid (h) | sc-408425-NIC | 20 µg | $410.00 | |||
ABHD7 Double Nickase Plasmid (h2) | sc-408425-NIC-2 | 20 µg | $410.00 |
Human ABHD7 (also referenced with EPHX4) encodes an α/β-hydrolase domain–containing serine hydrolase that is predicted to participate in lipid and ester metabolism within cellular membranes. As a member of the broader serine hydrolase network, ABHD7 activity can influence lipid signaling dynamics, membrane homeostasis, and metabolic crosstalk that modulates stress responses and inflammatory signaling. Altered regulation of lipid-metabolic enzymes is frequently associated with dysregulated proliferation, oxidative stress handling, and changes in cell-state transitions, making ABHD7 a relevant node for mechanistic studies in metabolic and signaling rewiring. Profiling ABHD7 function supports research into enzyme-linked lipid pathways and their connections to disease-associated cellular phenotypes in human models.
ABHD7 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the EPHX4 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within EPHX4. 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 EPHX4 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 EPHX4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.