Grx2 Double Nickase Plasmid (h): sc-412093-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Grx2 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
- Grx2 Double Nickase Plasmid (h) and Grx2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GLRX2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Grx2 Double Nickase Plasmid (h) | sc-412093-NIC | 20 µg | $410.00 |
Human GLRX2 encodes glutaredoxin-2 (Grx2), a thiol–disulfide oxidoreductase that uses glutathione to catalyze reversible protein deglutathionylation and maintain mitochondrial and cytosolic redox homeostasis. Grx2 modulates reactive oxygen species handling, supports mitochondrial integrity, and influences redox-sensitive processes including apoptosis, iron–sulfur cluster biogenesis, and metabolic enzyme activity. Through these functions, GLRX2 is positioned within oxidative stress response networks and glutathione-dependent signaling pathways that shape cellular adaptation to redox imbalance. Altered redox control involving GLRX2 has been studied in contexts of mitochondrial dysfunction and oxidative damage relevant to neurodegeneration, cardiometabolic stress, and cancer cell survival mechanisms.
Grx2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GLRX2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GLRX2. 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 GLRX2 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 GLRX2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.