ACBP Double Nickase Plasmid (h): sc-402557-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACBP 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
- ACBP Double Nickase Plasmid (h) and ACBP Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DBI. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ACBP Antibody (C-9): sc-376853
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACBP Double Nickase Plasmid (h) | sc-402557-NIC | 20 µg | $410.00 | |||
ACBP Double Nickase Plasmid (h2) | sc-402557-NIC-2 | 20 µg | $410.00 |
Human DBI encodes acyl-CoA–binding protein (ACBP), a small cytosolic lipid chaperone that binds long-chain acyl-CoA esters and buffers their availability for lipid synthesis, β-oxidation, and membrane remodeling. By regulating acyl-CoA trafficking, ACBP influences metabolic homeostasis, ER stress responses, and coupling between lipid metabolism and signaling pathways that shape cellular energy balance. DBI/ACBP activity has been studied in contexts of metabolic dysregulation, lipid droplet biology, and stress-adaptive programs that are frequently altered in cancer and neurodegenerative disease models. As a multifunctional acyl-CoA carrier, ACBP provides a tractable node for dissecting how lipid availability rewires transcriptional and organelle-level phenotypes.
ACBP Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DBI locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DBI. 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 DBI 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 DBI-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.