CHCHD10 Double Nickase Plasmid (h): sc-407891-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CHCHD10 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
- CHCHD10 Double Nickase Plasmid (h) and CHCHD10 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CHCHD10. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CHCHD10 Double Nickase Plasmid (h) | sc-407891-NIC | 20 µg | $410.00 | |||
CHCHD10 Double Nickase Plasmid (h2) | sc-407891-NIC-2 | 20 µg | $410.00 |
CHCHD10 encodes a coiled-coil-helix–coiled-coil-helix domain–containing protein that localizes to mitochondria and supports mitochondrial cristae integrity and respiratory chain function. It participates in pathways governing oxidative phosphorylation, mitochondrial dynamics, and cellular stress responses, influencing bioenergetic homeostasis and apoptosis susceptibility. Dysregulation or mutation of CHCHD10 has been linked to neurodegenerative phenotypes, including motor neuron and frontotemporal spectrum disorders, consistent with its role in maintaining mitochondrial proteostasis. As a result, CHCHD10 is widely studied in models of mitochondrial dysfunction, proteotoxic stress, and neuronally relevant energy metabolism.
CHCHD10 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CHCHD10 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CHCHD10. 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 CHCHD10 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 CHCHD10-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.