FUS/TLS Double Nickase Plasmid (h): sc-400612-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FUS/TLS 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
- FUS/TLS Double Nickase Plasmid (h) and FUS/TLS Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FUS. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: FUS/TLS Antibody (4H11): sc-47711
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FUS/TLS Double Nickase Plasmid (h) | sc-400612-NIC | 20 µg | $410.00 | |||
FUS/TLS Double Nickase Plasmid (h2) | sc-400612-NIC-2 | 20 µg | $410.00 |
FUS (FUS/TLS) encodes a multifunctional RNA/DNA-binding protein that shuttles between nucleus and cytoplasm to coordinate transcription, pre-mRNA splicing, RNA transport, and stress granule dynamics. FUS participates in the DNA damage response, including double-strand break repair, through interactions with RNA polymerase II and repair factors that influence genome stability. Dysregulation, mislocalization, or aggregation of FUS is linked to neurodegenerative disease biology, and altered FUS activity has also been implicated in oncogenic transcriptional programs. These properties make FUS a widely used node for studying RNA metabolism, proteostasis, and genotoxic stress signaling in human cells.
FUS/TLS Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FUS locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FUS. 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 FUS 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 FUS-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.