α-KGD Double Nickase Plasmid (h): sc-402915-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- α-KGD 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
- α-KGD Double Nickase Plasmid (h) and α-KGD Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting OGDH. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
α-KGD Double Nickase Plasmid (h) | sc-402915-NIC | 20 µg | $410.00 | |||
α-KGD Double Nickase Plasmid (h2) | sc-402915-NIC-2 | 20 µg | $410.00 |
Human OGDH encodes the E1 component of the 2-oxoglutarate dehydrogenase complex (α-KGD), a rate-influencing enzyme of the tricarboxylic acid (TCA) cycle that converts α-ketoglutarate to succinyl-CoA while generating NADH. This reaction integrates mitochondrial carbon flux with cellular redox balance and supports oxidative phosphorylation, anaplerosis, and amino acid metabolism through the α-ketoglutarate node. OGDH activity also links mitochondrial metabolism to reactive oxygen species handling and stress responses via NADH production and downstream electron transport. Dysregulation of OGDH/α-KGD-associated pathways has been implicated in metabolic remodeling observed in neurological disorders and cancer-related bioenergetic adaptation, making it a useful target for mechanistic studies of mitochondrial function.
α-KGD Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the OGDH locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within OGDH. 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 OGDH 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 OGDH-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.