FBXO38 Double Nickase Plasmid (m): sc-430688-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FBXO38 Double Nickase Plasmid (m) 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
- FBXO38 Double Nickase Plasmid (m) and FBXO38 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Fbxo38. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FBXO38 Double Nickase Plasmid (m) | sc-430688-NIC | 20 µg | $410.00 | |||
FBXO38 Double Nickase Plasmid (m2) | sc-430688-NIC-2 | 20 µg | $410.00 |
Mouse Fbxo38 encodes FBXO38, an F-box protein that is predicted to function as a substrate-recognition component of SCF (SKP1–CUL1–F-box) E3 ubiquitin ligase complexes, linking selected proteins to ubiquitination and proteasomal turnover. Through this role, FBXO38 is positioned to influence cellular proteostasis, cell-cycle control, and signal transduction pathways that depend on regulated protein stability. Altered F-box–mediated ubiquitin signaling is broadly associated with dysregulated proliferation, stress responses, and genome maintenance, making Fbxo38 a useful target for mechanistic studies in mouse systems. Investigating FBXO38-dependent ubiquitination networks can help clarify how targeted degradation modulates tissue homeostasis and disease-relevant cellular phenotypes.
FBXO38 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Fbxo38 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Fbxo38. 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 Fbxo38 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 Fbxo38-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.