OTUD2 Double Nickase Plasmid (h): sc-406672-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- OTUD2 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
- OTUD2 Double Nickase Plasmid (h) and OTUD2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting YOD1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
OTUD2 Double Nickase Plasmid (h) | sc-406672-NIC | 20 µg | $410.00 |
Human YOD1 encodes the deubiquitinating enzyme OTUD2, an OTU-domain cysteine protease that edits ubiquitin signals to regulate protein stability and signaling outputs. OTUD2 participates in ubiquitin-dependent control of proteostasis and stress responses, interfacing with pathways that govern endoplasmic reticulum–associated degradation, inflammatory signaling, and DNA damage-associated ubiquitin remodeling. By shaping the kinetics and specificity of ubiquitin chain removal, OTUD2 can influence transcriptional programs, cell-cycle progression, and apoptosis thresholds. Dysregulation of deubiquitination pathways involving OTUD2 has been associated with altered immune signaling and oncogenic phenotypes, motivating mechanistic studies in tumor biology and inflammation.
OTUD2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the YOD1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within YOD1. 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 YOD1 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 YOD1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.