UBXD4 Double Nickase Plasmid (h): sc-414883-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- UBXD4 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
- UBXD4 Double Nickase Plasmid (h) and UBXD4 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting UBXN2A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
UBXD4 Double Nickase Plasmid (h) | sc-414883-NIC | 20 µg | $410.00 | |||
UBXD4 Double Nickase Plasmid (h2) | sc-414883-NIC-2 | 20 µg | $410.00 |
UBXN2A encodes UBXD4, a UBX domain–containing cofactor that interfaces with the AAA+ ATPase p97/VCP to coordinate ubiquitin-dependent protein quality control. UBXD4 is implicated in endoplasmic reticulum–associated degradation, proteasome-linked turnover, and the maintenance of cellular proteostasis under stress conditions. Through these processes, UBXD4 can influence the stability of regulatory proteins and the resolution of misfolded or damaged protein species. Dysregulation of p97 adaptor networks and ubiquitin–proteasome pathways is broadly connected to neurodegenerative and cancer-associated proteostasis defects, making UBXN2A a relevant target for mechanistic studies.
UBXD4 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the UBXN2A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within UBXN2A. 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 UBXN2A 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 UBXN2A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.