Ubr4 Double Nickase Plasmid (m): sc-427303-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Ubr4 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
- Ubr4 Double Nickase Plasmid (m) and Ubr4 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ubr4. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Ubr4 Antibody (21-Y): sc-100615
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Ubr4 Double Nickase Plasmid (m) | sc-427303-NIC | 20 µg | $410.00 | |||
Ubr4 Double Nickase Plasmid (m2) | sc-427303-NIC-2 | 20 µg | $410.00 |
Mouse Ubr4 encodes an E3 ubiquitin ligase that participates in the N-end rule ubiquitin–proteasome pathway, linking substrate recognition to proteostasis and regulated protein turnover. UBR4 has been implicated in endocytic trafficking, membrane protein homeostasis, and broader ubiquitin-dependent control of cellular stress responses. Through these functions, UBR4 influences cell survival, differentiation, and neuronal and developmental processes where tightly controlled protein degradation is required. Dysregulation of ubiquitination and proteostasis networks involving UBR-family ligases is relevant to studies of neurobiology, cardiometabolic phenotypes, and cancer-associated signaling vulnerabilities in model systems.
Ubr4 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ubr4 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ubr4. 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 Ubr4 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 Ubr4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.