CLN5 Double Nickase Plasmid (h): sc-408473-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CLN5 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
- CLN5 Double Nickase Plasmid (h) and CLN5 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CLN5. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CLN5 Antibody (D-8): sc-374672
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CLN5 Double Nickase Plasmid (h) | sc-408473-NIC | 20 µg | $410.00 | |||
CLN5 Double Nickase Plasmid (h2) | sc-408473-NIC-2 | 20 µg | $410.00 |
CLN5 encodes a soluble lysosomal glycoprotein implicated in endolysosomal trafficking and proteostasis, supporting proper lysosome function and turnover of cellular macromolecules. CLN5 activity is linked to lysosome-related pathways including autophagy-lysosome flux, vesicle transport, and maintenance of neuronal homeostasis. Loss-of-function variants in CLN5 are associated with neuronal ceroid lipofuscinosis, characterized by lysosomal storage pathology and progressive neurodegeneration, making CLN5 a key target for studying lysosomal dysfunction mechanisms. In human cell models, CLN5 perturbation is commonly used to interrogate lysosomal enzyme processing, cargo sorting, and accumulation of storage material.
CLN5 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CLN5 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CLN5. 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 CLN5 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 CLN5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.