Syntaxin 17 Double Nickase Plasmid (h): sc-403251-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Syntaxin 17 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
- Syntaxin 17 Double Nickase Plasmid (h) and Syntaxin 17 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting STX17. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Syntaxin 17 Antibody (A-11): sc-518187
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Syntaxin 17 Double Nickase Plasmid (h) | sc-403251-NIC | 20 µg | $410.00 | |||
Syntaxin 17 Double Nickase Plasmid (h2) | sc-403251-NIC-2 | 20 µg | $410.00 |
STX17 encodes Syntaxin 17, an ER-anchored SNARE that localizes to mitochondria-associated membranes and autophagosomes, where it mediates late-stage autophagy by promoting autophagosome–lysosome fusion. Through interactions with SNAP29 and VAMP8, STX17 supports autophagic flux, organelle quality control, and cellular adaptation to nutrient stress, with downstream effects on mitochondrial homeostasis and innate immune signaling. Perturbation of STX17-dependent trafficking and autophagy has been linked to altered mitophagy and proteostasis imbalance, processes relevant to neurodegeneration, cancer cell stress tolerance, and inflammatory phenotypes. As a node at the interface of membrane fusion and selective autophagy, STX17 is frequently studied in pathways governing lysosomal function, mitochondrial turnover, and cell survival under stress.
Syntaxin 17 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the STX17 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within STX17. 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 STX17 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 STX17-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.