ALOXE3 Double Nickase Plasmid (h): sc-408487-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ALOXE3 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
- ALOXE3 Double Nickase Plasmid (h) and ALOXE3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ALOXE3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ALOXE3 Double Nickase Plasmid (h) | sc-408487-NIC | 20 µg | $410.00 |
ALOXE3 encodes arachidonate lipoxygenase 3, an epidermis-enriched enzyme that participates in oxidative metabolism of polyunsaturated fatty acids and contributes to the generation of lipid mediators involved in keratinocyte differentiation. In the skin barrier program, ALOXE3 functions alongside other lipoxygenases to support cornification processes and the formation of the stratum corneum, influencing epidermal lipid organization and permeability control. Disruption of ALOXE3 activity is linked to congenital ichthyosis phenotypes, reflecting impaired barrier formation and altered lipid processing. As a result, ALOXE3 is frequently studied in pathways connecting fatty-acid oxidation, epidermal differentiation, and inflammatory signaling in dermatologic disease models.
ALOXE3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ALOXE3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ALOXE3. 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 ALOXE3 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 ALOXE3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.