SETX Double Nickase Plasmid (h): sc-402354-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SETX 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
- SETX Double Nickase Plasmid (h) and SETX Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SETX. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: SETX Antibody (QQ-7): sc-100319
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SETX Double Nickase Plasmid (h) | sc-402354-NIC | 20 µg | $410.00 | |||
SETX Double Nickase Plasmid (h2) | sc-402354-NIC-2 | 20 µg | $410.00 |
SETX (senataxin) encodes a DNA/RNA helicase that resolves RNA:DNA hybrids (R-loops) and supports transcription termination, replication–transcription conflict resolution, and genome stability. The protein functions at sites of DNA damage and is linked to pathways including the DNA damage response, homologous recombination, and maintenance of telomere and replication fork integrity. Through these activities, SETX helps prevent accumulation of transcription-associated lesions and aberrant recombination events. Dysregulation or mutation of SETX is associated with neurodegeneration and genome instability phenotypes, making it a key target for mechanistic studies of RNA processing and DNA repair coupling.
SETX Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SETX locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SETX. 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 SETX 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 SETX-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.