OTUD7A Double Nickase Plasmid (h): sc-414831-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- OTUD7A 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
- OTUD7A Double Nickase Plasmid (h) and OTUD7A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting OTUD7A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
OTUD7A Double Nickase Plasmid (h) | sc-414831-NIC | 20 µg | $410.00 | |||
OTUD7A Double Nickase Plasmid (h2) | sc-414831-NIC-2 | 20 µg | $410.00 |
OTUD7A (OTU deubiquitinase 7A) is a human cysteine protease that removes ubiquitin from protein substrates, shaping ubiquitin-dependent signaling and protein turnover. Through regulation of deubiquitination, OTUD7A influences pathways linked to proteostasis, endosomal/vesicular trafficking, and stress-responsive signaling that affect cellular homeostasis. Genetic and functional studies have associated OTUD7A perturbation with neurodevelopmental phenotypes, supporting investigation into how altered ubiquitin dynamics impacts neuronal differentiation, synaptic function, and genome stability. As a deubiquitinase, OTUD7A is also relevant to research on ubiquitin chain editing and cross-talk between ubiquitination and other post-translational modifications.
OTUD7A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the OTUD7A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within OTUD7A. 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 OTUD7A 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 OTUD7A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.