WDR68 Double Nickase Plasmid (h): sc-409221-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- WDR68 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
- WDR68 Double Nickase Plasmid (h) and WDR68 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DCAF7. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
WDR68 Double Nickase Plasmid (h) | sc-409221-NIC | 20 µg | $410.00 | |||
WDR68 Double Nickase Plasmid (h2) | sc-409221-NIC-2 | 20 µg | $410.00 |
DCAF7 (WDR68) encodes a conserved WD-repeat scaffold protein that supports assembly of signaling complexes and coordinates kinase-driven regulation of transcriptional and developmental programs. WDR68 has been implicated in MAPK-related signaling and modulation of nuclear events through interactions with protein kinases and transcriptional regulators, linking extracellular cues to gene expression changes. By influencing protein complex stability and subcellular localization, WDR68 contributes to control of cell proliferation and differentiation. Dysregulation of WDR68-associated networks has been explored in the context of cancer-related signaling and other diseases where aberrant kinase and transcriptional pathways are involved.
WDR68 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DCAF7 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DCAF7. 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 DCAF7 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 DCAF7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.