ALX3 Double Nickase Plasmid (m): sc-419094-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ALX3 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
- ALX3 Double Nickase Plasmid (m) and ALX3 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Alx3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ALX3 Double Nickase Plasmid (m) | sc-419094-NIC | 20 µg | $410.00 |
ALX3 (aristaless-like homeobox 3) is a paired-type homeobox transcription factor that regulates developmental patterning programs in the craniofacial complex and limb, controlling transcriptional networks that coordinate cell fate decisions, proliferation, and morphogenesis. In mouse, Alx3 contributes to gene regulatory circuits governing neural crest–derived mesenchyme and epidermal differentiation, interfacing with broader developmental signaling pathways that shape anterior-posterior and dorsal-ventral patterning. Dysregulation of ALX family transcription factors is linked to congenital malformations of craniofacial and limb structures, making Alx3 a relevant locus for studying genotype–phenotype relationships in developmental biology. Its tightly controlled expression also provides a model for investigating how homeobox factors modulate chromatin state and lineage-specific transcription.
ALX3 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Alx3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Alx3. 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 Alx3 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 Alx3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.