IDH3A Double Nickase Plasmid (h): sc-404788-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IDH3A 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
- IDH3A Double Nickase Plasmid (h) and IDH3A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting IDH3A. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: IDH3A Antibody (A-10): sc-398021
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IDH3A Double Nickase Plasmid (h) | sc-404788-NIC | 20 µg | $410.00 | |||
IDH3A Double Nickase Plasmid (h2) | sc-404788-NIC-2 | 20 µg | $410.00 |
IDH3A encodes the alpha subunit of NAD-dependent isocitrate dehydrogenase 3, a core enzyme of the mitochondrial tricarboxylic acid (TCA) cycle that catalyzes the oxidative decarboxylation of isocitrate to α-ketoglutarate with concurrent NADH production. By coupling carbon flux to respiratory chain activity, IDH3A contributes to cellular energy metabolism, redox balance, and biosynthetic precursor availability. Altered IDH3A function can perturb mitochondrial metabolism and has been associated with disorders involving oxidative phosphorylation and tissue energy demand, supporting its relevance in studies of metabolic stress, mitochondrial signaling, and growth control.
IDH3A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the IDH3A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within IDH3A. 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 IDH3A 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 IDH3A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.