Haspin Double Nickase Plasmid (m): sc-420703-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Haspin 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
- Haspin Double Nickase Plasmid (m) and Haspin Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Gsg2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Haspin Double Nickase Plasmid (m) | sc-420703-NIC | 20 µg | $410.00 | |||
Haspin Double Nickase Plasmid (m2) | sc-420703-NIC-2 | 20 µg | $410.00 |
Mouse Gsg2 encodes Haspin, an atypical serine/threonine kinase that orchestrates mitotic chromosome dynamics by phosphorylating histone H3 at threonine 3, a modification that promotes chromosomal passenger complex recruitment and supports accurate sister chromatid cohesion and segregation. Through this H3T3 phosphorylation axis, Haspin interfaces with centromeric signaling networks involving Aurora B activity, spindle checkpoint control, and kinetochore–microtubule attachment stability. Perturbation of Haspin-dependent mitotic regulation can drive chromosomal instability and aneuploidy, linking Gsg2/Haspin function to pathways broadly relevant to genome maintenance and proliferative stress. As a result, Gsg2 is frequently studied in cell cycle regulation, chromatin phosphorylation crosstalk, and mechanistic models of mitotic fidelity in mammalian cells.
Haspin Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Gsg2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Gsg2. 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 Gsg2 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 Gsg2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.