HIGD2A Double Nickase Plasmid (h): sc-406650-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HIGD2A 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
- HIGD2A Double Nickase Plasmid (h) and HIGD2A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HIGD2A. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: HIGD2A Antibody (A-6): sc-390505
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HIGD2A Double Nickase Plasmid (h) | sc-406650-NIC | 20 µg | $410.00 |
HIGD2A (hypoxia inducible domain family member 2A) encodes a small inner mitochondrial membrane protein that supports oxidative phosphorylation by promoting cytochrome c oxidase (Complex IV) assembly and stability, particularly through regulation of COX3 module biogenesis. By influencing electron transport chain integrity, HIGD2A contributes to mitochondrial respiration, membrane potential maintenance, and cellular responses to metabolic and oxygen stress. Perturbation of HIGD2A function is expected to impact bioenergetic homeostasis, reactive oxygen species handling, and mitochondrial quality control pathways. These processes are frequently studied in the context of mitochondrial dysfunction and metabolic remodeling observed across a range of disease-relevant cellular phenotypes.
HIGD2A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HIGD2A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HIGD2A. 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 HIGD2A 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 HIGD2A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.