UCH-L5 Double Nickase Plasmid (h): sc-416520-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- UCH-L5 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
- UCH-L5 Double Nickase Plasmid (h) and UCH-L5 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting UCHL5. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: UCH-L5 Antibody (C-4): sc-271002
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
UCH-L5 Double Nickase Plasmid (h) | sc-416520-NIC | 20 µg | $410.00 | |||
UCH-L5 Double Nickase Plasmid (h2) | sc-416520-NIC-2 | 20 µg | $410.00 |
Human UCHL5 (UCH-L5/UCH37) is a deubiquitinating enzyme that removes ubiquitin from protein substrates to regulate proteostasis and ubiquitin-dependent signaling. It associates with the 19S regulatory particle of the proteasome and can also function in the INO80 chromatin remodeling context, linking deubiquitination to protein turnover and transcriptional control. By shaping ubiquitin chain editing and substrate processing, UCH-L5 influences cell-cycle progression, stress responses, and genome stability pathways. Dysregulated ubiquitin–proteasome system activity involving UCHL5 has been studied in the context of cancer biology and neurodegeneration-related proteostasis defects.
UCH-L5 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the UCHL5 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within UCHL5. 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 UCHL5 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 UCHL5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.