OTUB1 Double Nickase Plasmid (m): sc-430702-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- OTUB1 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
- OTUB1 Double Nickase Plasmid (m) and OTUB1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Otub1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: OTUB1 Antibody (J-61): sc-130458
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
OTUB1 Double Nickase Plasmid (m) | sc-430702-NIC | 20 µg | $410.00 | |||
OTUB1 Double Nickase Plasmid (m2) | sc-430702-NIC-2 | 20 µg | $410.00 |
Mouse Otub1 encodes OTUB1, an ovarian tumor (OTU) family deubiquitinase that edits ubiquitin chain architecture and suppresses ubiquitin-dependent signaling. OTUB1 regulates proteostasis and stress responses by modulating K48- and K63-linked ubiquitination, with well-described roles in the DNA damage response through regulation of ubiquitin signaling at double-strand breaks. By shaping ubiquitin-mediated pathway flux, OTUB1 influences cell-cycle progression, genome stability, and inflammatory signaling outputs. Dysregulated OTUB1 activity has been associated with aberrant signaling in cancer-relevant pathways and altered immune and neurobiological processes, supporting its study in disease-modeling contexts.
OTUB1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Otub1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Otub1. 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 Otub1 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 Otub1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.