ESD Double Nickase Plasmid (h): sc-404314-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ESD 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
- ESD Double Nickase Plasmid (h) and ESD Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ESD. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ESD Antibody (A-5): sc-514892
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ESD Double Nickase Plasmid (h) | sc-404314-NIC | 20 µg | $410.00 | |||
ESD Double Nickase Plasmid (h2) | sc-404314-NIC-2 | 20 µg | $410.00 |
Human ESD encodes S-formylglutathione hydrolase, a serine hydrolase that functions in formaldehyde detoxification within the glutathione-dependent alcohol/aldehyde metabolism pathway. By hydrolyzing S-formylglutathione to glutathione and formate, ESD supports cellular redox balance and limits accumulation of reactive carbonyl species that can damage proteins and nucleic acids. ESD activity intersects with oxidative stress responses and broader metabolic homeostasis, linking perturbations in aldehyde handling to genotoxic stress and altered cell viability. Dysregulated carbonyl detoxification capacity has been investigated in contexts where oxidative and aldehyde stress contribute to disease-associated phenotypes, including metabolic and neurodegenerative processes.
ESD Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ESD locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ESD. 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 ESD 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 ESD-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.