HAX-1 Double Nickase Plasmid (m): sc-423888-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HAX-1 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
- HAX-1 Double Nickase Plasmid (m) and HAX-1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Hax1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HAX-1 Double Nickase Plasmid (m) | sc-423888-NIC | 20 µg | $410.00 | |||
HAX-1 Double Nickase Plasmid (m2) | sc-423888-NIC-2 | 20 µg | $410.00 |
Mouse Hax1 encodes HAX-1, a predominantly mitochondrial and endoplasmic reticulum–associated protein that modulates cell survival, calcium homeostasis, and cytoskeletal dynamics. HAX-1 participates in intrinsic apoptosis control by influencing mitochondrial membrane integrity and caspase-dependent signaling, and it has been linked to regulation of cell motility through interactions with actin-associated factors. In hematopoietic and immune contexts, altered HAX-1 function is associated with defects in granulocyte survival and differentiation, making it relevant to studies of neutrophil homeostasis and inflammatory responses. Its broader roles in stress signaling and mitochondrial physiology also connect HAX-1 to mechanisms that support tissue maintenance and degeneration under cellular stress.
HAX-1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Hax1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Hax1. 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 Hax1 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 Hax1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.