Calpain 10 Double Nickase Plasmid (h): sc-405032-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Calpain 10 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
- Calpain 10 Double Nickase Plasmid (h) and Calpain 10 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CAPN10. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Calpain 10 Double Nickase Plasmid (h) | sc-405032-NIC | 20 µg | $410.00 | |||
Calpain 10 Double Nickase Plasmid (h2) | sc-405032-NIC-2 | 20 µg | $410.00 |
CAPN10 encodes calpain 10, an atypical, calcium-regulated cysteine protease implicated in limited proteolysis that modulates protein turnover, cytoskeletal dynamics, and signal transduction. Calpain 10 has been linked to mitochondrial homeostasis, insulin signaling, and metabolic stress responses, influencing processes such as glucose utilization and cellular adaptation to nutrient status. Genetic variation and altered CAPN10 activity have been associated with susceptibility to metabolic phenotypes including insulin resistance and type 2 diabetes–related traits, supporting its relevance in metabolic disease biology. In cellular models, CAPN10 perturbation is used to interrogate protease-dependent regulation of organelle function, stress signaling, and pathway rewiring.
Calpain 10 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CAPN10 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CAPN10. 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 CAPN10 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 CAPN10-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.