CLN2 Double Nickase Plasmid (h): sc-405204-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CLN2 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
- CLN2 Double Nickase Plasmid (h) and CLN2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TPP1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CLN2 Antibody (G-3): sc-393961
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CLN2 Double Nickase Plasmid (h) | sc-405204-NIC | 20 µg | $410.00 | |||
CLN2 Double Nickase Plasmid (h2) | sc-405204-NIC-2 | 20 µg | $410.00 |
TPP1 encodes the lysosomal serine protease tripeptidyl peptidase 1 (CLN2), which removes N‑terminal tripeptides from polypeptides to support lysosomal protein turnover and cellular proteostasis. CLN2 function integrates with endo‑lysosomal trafficking, autophagy–lysosome pathways, and catabolic processing of substrates destined for degradation. Loss or dysfunction of TPP1 perturbs lysosomal homeostasis, promotes accumulation of undegraded material, and disrupts neuronal and glial resilience in models of lysosomal storage biology. Accordingly, TPP1/CLN2 is widely used as a mechanistic entry point for studying lysosome-dependent clearance pathways and disease-relevant cellular stress responses.
CLN2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TPP1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TPP1. 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 TPP1 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 TPP1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.