SCYL1 Double Nickase Plasmid (m): sc-429734-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SCYL1 Double Nickase Plasmid (m) 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
- SCYL1 Double Nickase Plasmid (m) and SCYL1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Scyl1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: SCYL1 Antibody (KA.72): sc-130466
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SCYL1 Double Nickase Plasmid (m) | sc-429734-NIC | 20 µg | $410.00 |
Mouse Scyl1 encodes SCYL1, an evolutionarily conserved pseudokinase-like protein that functions as a scaffold in membrane trafficking and proteostasis. SCYL1 localizes to the Golgi/ER interface and associates with COPI-mediated retrograde transport and ARF-dependent vesicle dynamics, supporting proper cargo retrieval and organelle homeostasis. Through links to RNA metabolism, protein quality control, and stress-adaptive signaling, SCYL1 contributes to neuronal and hepatic cellular resilience under physiological demand. Disruption of SCYL1 function has been associated with neurodegeneration and liver pathology in model systems, making it relevant for studies of intracellular transport defects and stress-related disease mechanisms.
SCYL1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Scyl1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Scyl1. 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 Scyl1 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 Scyl1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.