TPCN2 Double Nickase Plasmid (h): sc-402960-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TPCN2 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
- TPCN2 Double Nickase Plasmid (h) and TPCN2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TPCN2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TPCN2 Double Nickase Plasmid (h) | sc-402960-NIC | 20 µg | $410.00 | |||
TPCN2 Double Nickase Plasmid (h2) | sc-402960-NIC-2 | 20 µg | $410.00 |
Human TPCN2 (two-pore segment channel 2) encodes a NAADP-sensitive endolysosomal cation channel that regulates Ca²⁺ release from acidic organelles, coupling luminal ion homeostasis to cytosolic Ca²⁺ signaling. TPCN2 activity influences endosome–lysosome trafficking, autophagy-lysosome function, vesicular fusion, and nutrient-responsive pathways including mTOR signaling. Through these processes, TPCN2 has been studied in the context of pigmentation biology, metabolic regulation, and cellular responses to stress that depend on lysosomal signaling dynamics. Dysregulated endolysosomal Ca²⁺ handling linked to TPCN2 function is also relevant to models of neurodegeneration and pathogen entry where intracellular membrane trafficking is a key determinant.
TPCN2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TPCN2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TPCN2. 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 TPCN2 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 TPCN2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.