Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
HADHA Double Nickase Plasmid (h): sc-402803-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HADHA 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
- HADHA Double Nickase Plasmid (h) and HADHA Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HADHA. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: HADHA Antibody (E-8): sc-374497
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HADHA Double Nickase Plasmid (h) | sc-402803-NIC | 20 µg | $410.00 | |||
HADHA Double Nickase Plasmid (h2) | sc-402803-NIC-2 | 20 µg | $410.00 |
HADHA encodes the mitochondrial trifunctional protein alpha subunit, a core component of fatty acid β-oxidation that catalyzes the enoyl-CoA hydratase and 3-hydroxyacyl-CoA dehydrogenase steps required for long-chain fatty acyl-CoA metabolism. Through coupling with HADHB, HADHA supports energy homeostasis during fasting and high oxidative demand, linking lipid catabolism to mitochondrial function and redox balance. Disruption of HADHA is associated with mitochondrial fatty acid oxidation disorders, including long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency and mitochondrial trifunctional protein deficiency, which can manifest with cardiomyopathy, hypoketotic hypoglycemia, and myopathy. HADHA is therefore widely studied in metabolic stress responses, mitochondrial proteostasis, and lipid-driven signaling relevant to neuromuscular and cardiac biology.
HADHA Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HADHA locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HADHA. 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 HADHA 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 HADHA-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.