ACBD6 Double Nickase Plasmid (h): sc-413630-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACBD6 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
- ACBD6 Double Nickase Plasmid (h) and ACBD6 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ACBD6. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACBD6 Double Nickase Plasmid (h) | sc-413630-NIC | 20 µg | $410.00 | |||
ACBD6 Double Nickase Plasmid (h2) | sc-413630-NIC-2 | 20 µg | $410.00 |
ACBD6 encodes an acyl-CoA binding domain–containing protein implicated in intracellular lipid handling through binding of medium- to long-chain acyl-CoA esters and coordination of acyl-group trafficking. In human cells, ACBD6 has been linked to peroxisome-associated lipid metabolism and membrane lipid homeostasis, processes that influence energy balance, organelle function, and cellular stress responses. By shaping acyl-CoA availability, ACBD6 can affect downstream pathways including fatty acid remodeling, lipid signaling, and protein acylation-dependent regulation. Dysregulation of lipid metabolic networks in which ACBD6 participates is relevant to mechanistic studies of metabolic phenotypes and lipid-driven cellular dysfunction.
ACBD6 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ACBD6 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ACBD6. 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 ACBD6 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 ACBD6-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.