WDSOF1 Double Nickase Plasmid (h): sc-411819-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- WDSOF1 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
- WDSOF1 Double Nickase Plasmid (h) and WDSOF1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DCAF13. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
WDSOF1 Double Nickase Plasmid (h) | sc-411819-NIC | 20 µg | $410.00 |
Human DCAF13 (also known as WDSOF1) encodes a DDB1- and CUL4-associated factor that is thought to act as a substrate receptor within CUL4–DDB1 E3 ubiquitin ligase complexes, supporting selective ubiquitination and proteostasis. Through ubiquitin-dependent control of protein stability, DCAF13 can influence cell-cycle progression, nuclear organization, and stress-responsive signaling programs. Altered regulation of ubiquitin ligase pathways is frequently linked to dysregulated proliferation and genome maintenance, making DCAF13 a relevant target for mechanistic studies of growth control and proteome remodeling. In biomedical research contexts, perturbation of DCAF13 is used to interrogate how CUL4/DDB1-dependent ubiquitination interfaces with transcriptional regulation and cellular fitness.
WDSOF1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DCAF13 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DCAF13. 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 DCAF13 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 DCAF13-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.