USP2 Double Nickase Plasmid (m): sc-424700-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- USP2 Double Nickase Plasmid (m) 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
- USP2 Double Nickase Plasmid (m) and USP2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Usp2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
USP2 Double Nickase Plasmid (m) | sc-424700-NIC | 20 µg | $410.00 | |||
USP2 Double Nickase Plasmid (m2) | sc-424700-NIC-2 | 20 µg | $410.00 |
Usp2 encodes ubiquitin-specific peptidase 2 (USP2), a deubiquitinating enzyme that reverses ubiquitin-dependent protein turnover and modulates substrate stability across multiple cellular programs. USP2 has been linked to regulation of cell-cycle progression, apoptosis, and stress-responsive signaling, including crosstalk with inflammatory and metabolic pathways that rely on controlled ubiquitin editing. By shaping protein half-life and signaling amplitude, USP2 influences transcriptional outputs and cellular homeostasis in a context-dependent manner. Dysregulated USP2 activity or expression has been associated with disease-relevant phenotypes such as altered proliferation, immune signaling imbalance, and metabolic dysfunction, supporting its use as a mechanistic node in pathway studies.
USP2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Usp2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Usp2. 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 Usp2 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 Usp2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.