GSTM3 Double Nickase Plasmid (h): sc-404418-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GSTM3 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
- GSTM3 Double Nickase Plasmid (h) and GSTM3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GSTM3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GSTM3 Double Nickase Plasmid (h) | sc-404418-NIC | 20 µg | $410.00 | |||
GSTM3 Double Nickase Plasmid (h2) | sc-404418-NIC-2 | 20 µg | $410.00 |
Glutathione S-transferase mu 3 (GSTM3) is a cytosolic phase II detoxification enzyme that catalyzes glutathione conjugation to electrophilic compounds, supporting cellular defense against oxidative stress and xenobiotic insult. By modulating redox homeostasis and the handling of lipid peroxidation products, GSTM3 influences pathways linked to reactive oxygen species buffering, inflammatory signaling, and proteostasis. Variation in GSTM3 expression or activity has been associated with altered susceptibility to chemical-induced damage and interindividual differences in drug and environmental response, making it relevant to studies of toxicology and stress-adaptation biology. In cancer biology and chronic inflammatory contexts, GSTM3 is frequently investigated for its impact on tumor cell stress tolerance and metabolism-associated phenotypes.
GSTM3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GSTM3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GSTM3. 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 GSTM3 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 GSTM3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.