FTβ Double Nickase Plasmid (h): sc-403479-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FTβ 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
- FTβ Double Nickase Plasmid (h) and FTβ Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FNTB. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: FTβ Antibody (B-7): sc-46664
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FTβ Double Nickase Plasmid (h) | sc-403479-NIC | 20 µg | $410.00 | |||
FTβ Double Nickase Plasmid (h2) | sc-403479-NIC-2 | 20 µg | $410.00 |
FNTB encodes the β subunit of protein farnesyltransferase (FTβ), a key enzyme in the prenylation pathway that catalyzes farnesyl group transfer to C-terminal CAAX motif proteins. This lipid modification promotes membrane association, protein stability, and subcellular trafficking of diverse signaling proteins, thereby influencing pathways controlling proliferation, differentiation, and vesicular transport. FTβ-dependent farnesylation is closely linked to small GTPase-driven signal transduction networks and cytoskeletal regulation. Dysregulated prenylation dynamics and altered dependence on farnesyltransferase activity have been associated with oncogenic signaling contexts and other disorders involving aberrant membrane-localized signaling complexes.
FTβ Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FNTB locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FNTB. 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 FNTB 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 FNTB-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.