SAK/STK18/PLK4 Double Nickase Plasmid (m): sc-423195-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SAK/STK18/PLK4 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
- SAK/STK18/PLK4 Double Nickase Plasmid (m) and SAK/STK18/PLK4 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Plk4. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SAK/STK18/PLK4 Double Nickase Plasmid (m) | sc-423195-NIC | 20 µg | $410.00 | |||
SAK/STK18/PLK4 Double Nickase Plasmid (m2) | sc-423195-NIC-2 | 20 µg | $410.00 |
Mouse Plk4 encodes a serine/threonine kinase also known as SAK/STK18/PLK4 that functions as a master regulator of centriole biogenesis and centrosome duplication. PLK4 activity coordinates recruitment and phosphorylation of centriole assembly factors, linking the centrosome cycle to cell-cycle progression and mitotic spindle organization. Dysregulated PLK4 levels can drive centriole overduplication, supernumerary centrosomes, and chromosomal instability, processes frequently studied in models of aneuploidy, tumorigenesis, and neurodevelopmental phenotypes. As a signaling hub at the centrosome, PLK4 is commonly investigated in pathways governing mitotic fidelity, checkpoint control, and microtubule-dependent organization.
SAK/STK18/PLK4 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Plk4 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Plk4. 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 Plk4 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 Plk4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.