GCDH Double Nickase Plasmid (h): sc-405887-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GCDH 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
- GCDH Double Nickase Plasmid (h) and GCDH Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GCDH. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GCDH Double Nickase Plasmid (h) | sc-405887-NIC | 20 µg | $410.00 | |||
GCDH Double Nickase Plasmid (h2) | sc-405887-NIC-2 | 20 µg | $410.00 |
Human GCDH encodes glutaryl‑CoA dehydrogenase, a mitochondrial FAD-dependent enzyme that catalyzes the oxidative decarboxylation step in lysine, hydroxylysine, and tryptophan catabolism. By funneling glutaryl‑CoA toward downstream acyl‑CoA metabolism, GCDH supports mitochondrial redox balance and interfaces with electron transfer flavoprotein–linked fatty acid and amino acid oxidation pathways. Loss of GCDH activity is associated with disruptions in organic acid handling and mitochondrial stress responses that are relevant to inborn errors of metabolism such as glutaric acidemia type I. As a result, GCDH is frequently studied in the context of mitochondrial function, metabolite-driven toxicity, and pathway-level remodeling in metabolic disease models.
GCDH Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GCDH locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GCDH. 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 GCDH 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 GCDH-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.