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 Peroxidase 4/GPX4 Double Nickase Plasmid (m): sc-436949-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Glutathione Peroxidase 4/GPX4 Double Nickase Plasmid (m) 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 Peroxidase 4/GPX4 Double Nickase Plasmid (m) and Glutathione Peroxidase 4/GPX4 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Gpx4. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Glutathione Peroxidase 4/GPX4 Antibody (E-12): sc-166570
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Glutathione Peroxidase 4/GPX4 Double Nickase Plasmid (m) | sc-436949-NIC | 20 µg | $410.00 |
Mouse Gpx4 encodes glutathione peroxidase 4 (GPX4), a selenoenzyme that reduces phospholipid hydroperoxides within cellular membranes using glutathione, thereby preserving membrane integrity and redox homeostasis. GPX4 is a central suppressor of ferroptosis by limiting iron-driven lipid peroxidation and intersects with antioxidant networks such as glutathione metabolism and the NRF2-regulated oxidative stress response. Perturbation of GPX4 function alters mitochondrial and lipid signaling, influences inflammatory stress responses, and impacts cellular survival under oxidative and metabolic stress. Dysregulated GPX4 activity has been implicated in experimental models of neurodegeneration, ischemia-reperfusion injury, and tumor biology through its control of lipid peroxidation and ferroptotic sensitivity.
Glutathione Peroxidase 4/GPX4 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Gpx4 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Gpx4. 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 Gpx4 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 Gpx4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.