ABHD15 Double Nickase Plasmid (m): sc-426589-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ABHD15 Double Nickase Plasmid (m) 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
- ABHD15 Double Nickase Plasmid (m) and ABHD15 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Abhd15. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ABHD15 Double Nickase Plasmid (m) | sc-426589-NIC | 20 µg | $410.00 |
Abhd15 encodes ABHD15, an α/β-hydrolase domain–containing protein implicated in metabolic regulation and insulin-responsive signaling, with reported roles in modulating adipocyte function and energy homeostasis. In mouse systems, ABHD15 has been linked to pathways that influence glucose handling and lipid metabolism, including crosstalk with phosphodiesterase-regulated cAMP signaling that can shape adipogenesis and insulin sensitivity. Perturbation of Abhd15 expression is therefore relevant for mechanistic studies of metabolic phenotypes such as obesity-associated insulin resistance and related inflammatory remodeling in adipose tissue. These features make ABHD15 a useful target for dissecting gene networks that coordinate nutrient sensing, intracellular second-messenger signaling, and systemic metabolic adaptation.
ABHD15 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Abhd15 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Abhd15. 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 Abhd15 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 Abhd15-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.