FBL16 Double Nickase Plasmid (h): sc-414575-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FBL16 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
- FBL16 Double Nickase Plasmid (h) and FBL16 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FBXL16. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FBL16 Double Nickase Plasmid (h) | sc-414575-NIC | 20 µg | $410.00 | |||
FBL16 Double Nickase Plasmid (h2) | sc-414575-NIC-2 | 20 µg | $410.00 |
FBXL16 (FBL16) encodes an F-box protein that is predicted to function as a substrate-recognition component of SCF (SKP1–CUL1–RBX1) E3 ubiquitin ligase complexes, thereby influencing ubiquitin-dependent proteasomal turnover of target proteins. Through this role, FBXL16 is linked to regulation of protein homeostasis and cellular signaling outputs that depend on timely degradation of pathway effectors. Modulation of SCF/F-box activity can affect cell-cycle progression, stress responses, and transcriptional programs by altering stability of regulatory proteins. Dysregulation of ubiquitin–proteasome pathway components, including F-box adaptors, is frequently associated with altered signaling states observed in cancer and other disorders characterized by proteostasis imbalance.
FBL16 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FBXL16 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FBXL16. 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 FBXL16 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 FBXL16-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.