ABHD12 Double Nickase Plasmid (m): sc-429273-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ABHD12 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
- ABHD12 Double Nickase Plasmid (m) and ABHD12 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Abhd12. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ABHD12 Double Nickase Plasmid (m) | sc-429273-NIC | 20 µg | $410.00 |
Mouse Abhd12 encodes ABHD12, a membrane-associated serine hydrolase that functions as a lysophosphatidylserine lipase to regulate bioactive lipid pools and lipid-mediated signaling in the nervous and immune systems. By controlling lysophosphatidylserine turnover, ABHD12 influences microglial activation states, neuroinflammatory tone, and broader phospholipid remodeling processes linked to cellular homeostasis. Genetic disruption of ABHD12 is associated with neurodegenerative phenotypes in model systems, making Abhd12 a relevant node for studying lipid dysregulation, neuroinflammation, and neuronal maintenance pathways. ABHD12 research is frequently applied to interrogate lipid signaling networks that couple membrane metabolism to immune and neuronal function.
ABHD12 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Abhd12 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Abhd12. 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 Abhd12 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 Abhd12-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.