ARL3 Double Nickase Plasmid (h): sc-416856-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ARL3 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
- ARL3 Double Nickase Plasmid (h) and ARL3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ARL3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ARL3 Double Nickase Plasmid (h) | sc-416856-NIC | 20 µg | $410.00 | |||
ARL3 Double Nickase Plasmid (h2) | sc-416856-NIC-2 | 20 µg | $410.00 |
ARL3 encodes ADP-ribosylation factor-like GTPase 3, a small regulatory GTPase that cycles between GDP- and GTP-bound states to coordinate ciliary and photoreceptor trafficking. In the primary cilium, ARL3 functions with ARL13B and the GEF activity of ARL13B to control release and targeting of lipidated cargo via carriers such as UNC119 and PDE6D, supporting microtubule-based transport and ciliary membrane composition. Through these processes, ARL3 contributes to ciliogenesis, signal transduction, and compartmentalization of prenylated and myristoylated proteins. Dysregulation of ARL3-dependent trafficking is linked to cilia-associated phenotypes, including inherited retinal degeneration and broader ciliopathy-related mechanisms relevant to neurodevelopmental and sensory biology.
ARL3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ARL3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ARL3. 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 ARL3 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 ARL3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.