USP3 Double Nickase Plasmid (h): sc-404849-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- USP3 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
- USP3 Double Nickase Plasmid (h) and USP3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting USP3. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: USP3 Antibody (8L8): sc-135597
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
USP3 Double Nickase Plasmid (h) | sc-404849-NIC | 20 µg | $410.00 | |||
USP3 Double Nickase Plasmid (h2) | sc-404849-NIC-2 | 20 µg | $410.00 |
Human USP3 encodes a ubiquitin-specific protease that reverses ubiquitination to regulate protein stability and signaling fidelity. USP3 is best known for deubiquitinating chromatin-associated substrates and coordinating genome maintenance programs, linking ubiquitin signaling to DNA replication stress responses and DNA damage repair. Through these activities, USP3 influences cell-cycle progression and chromatin dynamics, processes frequently perturbed in proliferative disorders and tumor biology. Altered USP3 expression or function has been associated with dysregulated ubiquitin homeostasis and genome instability phenotypes relevant to mechanistic studies in cancer and other diseases involving impaired DNA repair.
USP3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the USP3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within USP3. 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 USP3 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 USP3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.