Sil Double Nickase Plasmid (h): sc-409193-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Sil 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
- Sil Double Nickase Plasmid (h) and Sil Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting STIL. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Sil Antibody (A-6): sc-271910
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Sil Double Nickase Plasmid (h) | sc-409193-NIC | 20 µg | $410.00 |
STIL (SCL/TAL1 interrupting locus), also known as Sil, encodes a centrosomal protein required for centriole biogenesis and proper mitotic spindle assembly. It functions in the PLK4–STIL–SAS-6 axis to initiate procentriole formation, supporting accurate chromosome segregation and cell-cycle progression. Through its roles in centrosome duplication and neurodevelopmental processes, altered STIL activity is linked to centrosome amplification, proliferative dysregulation, and developmental disorders such as primary microcephaly. These features make STIL a widely used target for studying centrosome homeostasis, mitotic fidelity, and genotype-to-phenotype relationships in proliferating human cells.
Sil Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the STIL locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within STIL. 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 STIL 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 STIL-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.