FBXO10 Double Nickase Plasmid (h): sc-406159-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FBXO10 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
- FBXO10 Double Nickase Plasmid (h) and FBXO10 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FBXO10. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FBXO10 Double Nickase Plasmid (h) | sc-406159-NIC | 20 µg | $410.00 | |||
FBXO10 Double Nickase Plasmid (h2) | sc-406159-NIC-2 | 20 µg | $410.00 |
FBXO10 encodes an F-box substrate receptor within SKP1–CUL1–F-box (SCF) E3 ubiquitin ligase complexes, linking specific proteins to ubiquitination and proteasome-dependent turnover. Through regulated degradation of signaling and cell-fate determinants, FBXO10 contributes to control of apoptosis, protein homeostasis, and downstream stress-response pathways. Altered FBXO10 function or expression has been associated with dysregulated survival signaling and has been studied in the context of lymphoid malignancy biology, where ubiquitin-mediated proteostasis is frequently perturbed. As a result, FBXO10 is a useful target for interrogating ubiquitin–proteasome pathway wiring and its impact on cellular fitness and differentiation programs.
FBXO10 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FBXO10 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FBXO10. 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 FBXO10 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 FBXO10-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.