PRDM9 Double Nickase Plasmid (h): sc-412740-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PRDM9 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
- PRDM9 Double Nickase Plasmid (h) and PRDM9 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PRDM9. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PRDM9 Double Nickase Plasmid (h) | sc-412740-NIC | 20 µg | $410.00 | |||
PRDM9 Double Nickase Plasmid (h2) | sc-412740-NIC-2 | 20 µg | $410.00 |
PRDM9 encodes a meiosis-specific histone lysine methyltransferase and DNA-binding factor that specifies recombination hotspot locations by recognizing sequence motifs and depositing H3K4me3 and H3K36me3 marks. Through its KRAB, PR/SET, and zinc-finger domains, PRDM9 coordinates chromatin remodeling and recruitment of the meiotic recombination machinery to initiate programmed double-strand break formation and proper homologous chromosome pairing. Variation in PRDM9 zinc-finger arrays is a major determinant of hotspot usage and crossover distribution, linking PRDM9 function to genome stability and reproductive biology. Dysregulated PRDM9 activity or ectopic expression has also been explored in the context of aberrant epigenetic patterning and genomic rearrangements, making it relevant for studies of mutational processes and germline integrity.
PRDM9 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PRDM9 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PRDM9. 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 PRDM9 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 PRDM9-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.