GPAM Double Nickase Plasmid (h): sc-403961-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GPAM 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
- GPAM Double Nickase Plasmid (h) and GPAM Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GPAM. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: GPAM Antibody (D-10): sc-398135
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GPAM Double Nickase Plasmid (h) | sc-403961-NIC | 20 µg | $410.00 | |||
GPAM Double Nickase Plasmid (h2) | sc-403961-NIC-2 | 20 µg | $410.00 |
GPAM (glycerol-3-phosphate acyltransferase, mitochondrial) encodes a key acyltransferase that catalyzes the initial committed step of de novo glycerolipid synthesis by converting glycerol-3-phosphate to lysophosphatidic acid. By controlling flux into phosphatidic acid, triacylglycerol, and downstream phospholipid pools, GPAM links mitochondrial lipid metabolism to cellular energy storage, membrane biogenesis, and lipid signaling. GPAM activity intersects with fatty acid uptake and β-oxidation balance, lipid droplet formation, and metabolic stress responses. Dysregulated GPAM expression or activity has been associated with altered hepatic and adipose lipid handling and is frequently studied in the context of insulin resistance, steatosis, and broader cardiometabolic phenotypes.
GPAM Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GPAM locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GPAM. 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 GPAM 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 GPAM-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.