ABHD6 Double Nickase Plasmid (h): sc-405114-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ABHD6 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
- ABHD6 Double Nickase Plasmid (h) and ABHD6 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ABHD6. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ABHD6 Double Nickase Plasmid (h) | sc-405114-NIC | 20 µg | $410.00 | |||
ABHD6 Double Nickase Plasmid (h2) | sc-405114-NIC-2 | 20 µg | $410.00 |
ABHD6 (abhydrolase domain containing 6) is a serine hydrolase that regulates lipid signaling by hydrolyzing the endocannabinoid 2-arachidonoylglycerol and related monoacylglycerols, thereby shaping cellular pools of arachidonic acid derivatives and downstream eicosanoid responses. Through its control of glycerolipid and endocannabinoid metabolism, ABHD6 influences membrane lipid remodeling, metabolic homeostasis, and signal transduction pathways linked to inflammation and neuromodulatory processes. Altered ABHD6 activity has been studied in contexts of metabolic dysregulation, neuroinflammation, and tumor-associated lipid rewiring, where lipid signaling can affect proliferation, migration, and immune interactions. These features make ABHD6 a useful target for dissecting lipid-driven phenotypes using genetic perturbation models in human cells.
ABHD6 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ABHD6 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ABHD6. 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 ABHD6 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 ABHD6-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.