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.
Glutathione reductase Double Nickase Plasmid (h): sc-417499-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Glutathione reductase 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
- Glutathione reductase Double Nickase Plasmid (h) and Glutathione reductase Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GSR. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Glutathione reductase Antibody (C-10): sc-133245
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Glutathione reductase Double Nickase Plasmid (h) | sc-417499-NIC | 20 µg | $410.00 | |||
Glutathione reductase Double Nickase Plasmid (h2) | sc-417499-NIC-2 | 20 µg | $410.00 |
Human GSR encodes glutathione reductase, a flavoprotein oxidoreductase that uses NADPH to reduce oxidized glutathione (GSSG) to reduced glutathione (GSH), maintaining cellular redox buffering capacity. By sustaining the GSH/GSSG ratio, GSR supports detoxification of reactive oxygen species and electrophiles, intersects with glutathione-dependent peroxidase activity, and contributes to redox control in mitochondria and cytosol. This enzyme is integrated with NADPH-producing metabolism such as the pentose phosphate pathway and helps preserve thiol homeostasis that influences protein folding, signaling, and antioxidant defenses. Altered glutathione recycling and redox imbalance are frequently studied in contexts including oxidative stress susceptibility, hemolytic phenotypes, metabolic dysfunction, and tumor biology, where GSR-dependent pathways can modulate cellular fitness and stress responses.
Glutathione reductase Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GSR locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GSR. 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 GSR 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 GSR-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.