HoxD13 Double Nickase Plasmid (h): sc-404471-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HoxD13 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
- HoxD13 Double Nickase Plasmid (h) and HoxD13 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HOXD13. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HoxD13 Double Nickase Plasmid (h) | sc-404471-NIC | 20 µg | $410.00 | |||
HoxD13 Double Nickase Plasmid (h2) | sc-404471-NIC-2 | 20 µg | $410.00 |
HOXD13 encodes HoxD13, a homeobox transcription factor that controls positional identity and patterning during embryonic development, with prominent roles in limb and distal appendage morphogenesis. HoxD13 binds DNA through its conserved homeodomain to coordinate gene regulatory networks that govern segmentation, chondrogenesis, and differentiation programs, integrating with broader HOX cluster regulation and morphogen signaling such as SHH and WNT during tissue patterning. Disruption or misregulation of HOXD13 alters developmental transcriptional programs and has been linked to congenital limb malformations including synpolydactyly, making it a valuable target for studying genotype-to-phenotype relationships in human developmental biology.
HoxD13 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HOXD13 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HOXD13. 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 HOXD13 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 HOXD13-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.