USP27X Double Nickase Plasmid (h): sc-407628-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- USP27X 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
- USP27X Double Nickase Plasmid (h) and USP27X Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting USP27X. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
USP27X Double Nickase Plasmid (h) | sc-407628-NIC | 20 µg | $410.00 | |||
USP27X Double Nickase Plasmid (h2) | sc-407628-NIC-2 | 20 µg | $410.00 |
USP27X encodes a ubiquitin-specific protease that removes ubiquitin chains from target proteins to regulate their stability, subcellular localization, and signaling output. As part of the deubiquitination machinery, USP27X contributes to proteostasis control and modulation of ubiquitin-dependent pathways that influence cell-cycle progression, stress responses, and transcriptional programs. Dysregulation of ubiquitin signaling and deubiquitinase activity is broadly implicated in genome maintenance defects and aberrant growth signaling, making USP27X a relevant node for mechanistic studies of ubiquitin-driven regulation. Human USP27X is therefore of interest in research on pathway rewiring and disease-associated perturbations of protein turnover.
USP27X Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the USP27X locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within USP27X. 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 USP27X 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 USP27X-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.