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.
HADHB Double Nickase Plasmid (h): sc-403234-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HADHB 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
- HADHB Double Nickase Plasmid (h) and HADHB Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HADHB. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: HADHB Antibody (E-1): sc-271495
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HADHB Double Nickase Plasmid (h) | sc-403234-NIC | 20 µg | $410.00 | |||
HADHB Double Nickase Plasmid (h2) | sc-403234-NIC-2 | 20 µg | $410.00 |
HADHB encodes the beta subunit of mitochondrial trifunctional protein, a core enzyme complex that catalyzes key steps of long-chain fatty acid β-oxidation, including long-chain 3-ketoacyl-CoA thiolase activity. Through its role in mitochondrial energy metabolism, HADHB contributes to maintaining cellular ATP production and lipid homeostasis, particularly under high fatty acid flux. Disruption of HADHB function is associated with inherited mitochondrial fatty acid oxidation disorders such as mitochondrial trifunctional protein deficiency and long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency, which can present with metabolic decompensation and cardiomyopathy. HADHB is therefore widely studied in pathways linking mitochondrial dysfunction, oxidative stress, and lipid-driven cellular injury.
HADHB Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HADHB locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HADHB. 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 HADHB 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 HADHB-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.