HoxA2 Double Nickase Plasmid (h): sc-403732-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HoxA2 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
- HoxA2 Double Nickase Plasmid (h) and HoxA2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HOXA2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HoxA2 Double Nickase Plasmid (h) | sc-403732-NIC | 20 µg | $410.00 | |||
HoxA2 Double Nickase Plasmid (h2) | sc-403732-NIC-2 | 20 µg | $410.00 |
HOXA2 encodes the homeobox transcription factor HoxA2, a sequence-specific DNA-binding regulator that helps establish anterior–posterior patterning and segmental identity during embryogenesis, particularly in hindbrain rhombomere development and derivatives of the second pharyngeal arch. HoxA2 integrates developmental cues with chromatin and transcriptional programs to control lineage specification, neuronal differentiation, and morphogenetic processes. Dysregulated HOXA2 expression has been reported in multiple cancer and differentiation contexts, where altered homeobox networks can perturb proliferation, invasion, and cell fate stability. As a developmental regulator, HOXA2 is frequently studied to map enhancer–promoter logic, transcriptional hierarchy, and epigenetic states that maintain tissue-specific gene expression.
HoxA2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HOXA2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HOXA2. 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 HOXA2 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 HOXA2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.