ACCβ Double Nickase Plasmid (h): sc-401903-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACCβ 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
- ACCβ Double Nickase Plasmid (h) and ACCβ Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ACACB. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ACCβ Antibody (F-9): sc-377313
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACCβ Double Nickase Plasmid (h) | sc-401903-NIC | 20 µg | $410.00 | |||
ACCβ Double Nickase Plasmid (h2) | sc-401903-NIC-2 | 20 µg | $410.00 |
ACACB encodes acetyl-CoA carboxylase beta (ACCβ), a biotin-dependent carboxylase that catalyzes the formation of malonyl-CoA at the outer mitochondrial membrane. By controlling malonyl-CoA levels, ACCβ regulates fatty acid β-oxidation through inhibition of CPT1, thereby linking nutrient sensing to mitochondrial fuel selection and cellular energy homeostasis. ACACB activity integrates with AMPK signaling, insulin-responsive metabolic programs, and lipid handling pathways that shape oxidative metabolism in muscle and other tissues. Dysregulated ACCβ function and malonyl-CoA flux are associated with metabolic phenotypes relevant to obesity, insulin resistance, and fatty liver biology, supporting mechanistic studies of lipid-driven cellular stress and inflammation.
ACCβ Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ACACB locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ACACB. 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 ACACB 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 ACACB-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.