ACSS2 Double Nickase Plasmid (h): sc-402873-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACSS2 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
- ACSS2 Double Nickase Plasmid (h) and ACSS2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ACSS2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ACSS2 Antibody (A-9): sc-398559
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACSS2 Double Nickase Plasmid (h) | sc-402873-NIC | 20 µg | $410.00 | |||
ACSS2 Double Nickase Plasmid (h2) | sc-402873-NIC-2 | 20 µg | $410.00 |
ACSS2 (acyl-CoA synthetase short-chain family member 2) catalyzes the conversion of acetate to acetyl-CoA, linking acetate utilization to central carbon metabolism and lipid biosynthesis. By supplying nucleocytosolic acetyl-CoA, ACSS2 supports protein acetylation and chromatin regulation, integrating nutrient availability with transcriptional control under metabolic stress. ACSS2 activity intersects with pathways governing fatty acid metabolism, autophagy, and hypoxia-adaptive responses, and its dysregulation has been investigated in metabolic reprogramming contexts. Altered acetate flux and acetyl-CoA homeostasis involving ACSS2 are associated with changes in epigenetic state and cell-state transitions relevant to proliferative and inflammatory disease biology.
ACSS2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ACSS2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ACSS2. 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 ACSS2 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 ACSS2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.