UBXN2B Double Nickase Plasmid (h): sc-407871-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- UBXN2B 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
- UBXN2B Double Nickase Plasmid (h) and UBXN2B Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting UBXN2B. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
UBXN2B Double Nickase Plasmid (h) | sc-407871-NIC | 20 µg | $410.00 | |||
UBXN2B Double Nickase Plasmid (h2) | sc-407871-NIC-2 | 20 µg | $410.00 |
UBXN2B (ubiquitin regulatory X domain-containing protein 2B) is a UBX-domain adaptor implicated in ubiquitin-dependent protein quality control and remodeling of protein complexes. Through interactions with AAA ATPases such as VCP/p97, UBXN2B is positioned to influence endoplasmic reticulum-associated degradation (ERAD), proteostasis, and stress-adaptive signaling linked to misfolded protein clearance. These processes intersect with cell cycle regulation, apoptosis, and inflammatory responses, making UBXN2B a relevant node for studying pathways perturbed in neurodegeneration, cancer biology, and other proteostasis-associated disorders. Human UBXN2B functional perturbation can therefore be used to dissect how ubiquitin-mediated turnover shapes signaling networks and cellular homeostasis.
UBXN2B Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the UBXN2B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within UBXN2B. 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 UBXN2B 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 UBXN2B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.