WRN Double Nickase Plasmid (h): sc-401860-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- WRN 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
- WRN Double Nickase Plasmid (h) and WRN Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting WRN. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: WRN Antibody (D-6): sc-376182
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
WRN Double Nickase Plasmid (h) | sc-401860-NIC | 20 µg | $410.00 | |||
WRN Double Nickase Plasmid (h2) | sc-401860-NIC-2 | 20 µg | $410.00 |
WRN encodes a RecQ family DNA helicase/exonuclease that coordinates DNA replication, recombination, and multiple DNA repair processes, including base excision repair and homologous recombination. WRN supports replication fork stability and participates in telomere maintenance, thereby contributing to genome integrity during S phase and in response to replication stress. Loss of WRN function is associated with Werner syndrome and is linked to premature cellular senescence, chromosomal instability, and altered DNA damage signaling. WRN is also studied for its role in microsatellite instability contexts and for pathway interactions with ATR/ATM signaling, PARP-dependent repair, and checkpoint control.
WRN Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the WRN locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within WRN. 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 WRN 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 WRN-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.