RNF122 Double Nickase Plasmid (h): sc-410134-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RNF122 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
- RNF122 Double Nickase Plasmid (h) and RNF122 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RNF122. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RNF122 Double Nickase Plasmid (h) | sc-410134-NIC | 20 µg | $410.00 |
RNF122 encodes a RING finger E3 ubiquitin ligase that promotes ubiquitin-dependent protein turnover and contributes to proteostasis by regulating substrate stability. As part of the ubiquitin–proteasome system, RNF122 is positioned to influence signaling outcomes by controlling the abundance of pathway components involved in stress responses and cell-state regulation. Altered E3 ligase activity and ubiquitination dynamics are broadly linked to dysregulated cell growth, inflammatory signaling, and neurobiology-relevant processes, making RNF122 a useful node for mechanistic studies. Investigating RNF122 function can help clarify how ubiquitin-mediated regulation shapes downstream transcriptional and metabolic programs in human cells.
RNF122 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RNF122 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RNF122. 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 RNF122 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 RNF122-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.