ECHS1 Double Nickase Plasmid (h): sc-406053-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ECHS1 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
- ECHS1 Double Nickase Plasmid (h) and ECHS1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ECHS1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ECHS1 Double Nickase Plasmid (h) | sc-406053-NIC | 20 µg | $410.00 | |||
ECHS1 Double Nickase Plasmid (h2) | sc-406053-NIC-2 | 20 µg | $410.00 |
ECHS1 encodes short-chain enoyl-CoA hydratase 1, a mitochondrial matrix enzyme that catalyzes the hydration of trans-2-enoyl-CoA intermediates during fatty acid β-oxidation and contributes to branched-chain amino acid catabolism. By supporting acetyl-CoA generation and mitochondrial energy metabolism, ECHS1 influences redox balance and the handling of lipid-derived substrates under metabolic stress. Disruption of ECHS1 activity has been linked to mitochondrial dysfunction and inborn errors of metabolism with neurometabolic manifestations, making it relevant to studies of oxidative phosphorylation coupling, metabolite accumulation, and cellular bioenergetics. ECHS1 is therefore a useful target for investigating mitochondrial pathway crosstalk with stress signaling, lipid metabolism, and metabolic remodeling in human cells.
ECHS1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ECHS1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ECHS1. 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 ECHS1 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 ECHS1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.