MINOS1 Double Nickase Plasmid (h): sc-417564-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MINOS1 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
- MINOS1 Double Nickase Plasmid (h) and MINOS1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MINOS1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MINOS1 Double Nickase Plasmid (h) | sc-417564-NIC | 20 µg | $410.00 |
MINOS1 (mitochondrial inner membrane organizing system 1) encodes a core component of the MICOS complex that helps shape cristae architecture and maintain inner mitochondrial membrane organization. By supporting proper assembly of respiratory chain supercomplexes and intermembrane contact sites, MINOS1 contributes to oxidative phosphorylation efficiency, mitochondrial protein import, and organelle dynamics. Disruption of MICOS-associated factors, including MINOS1, is linked to altered mitochondrial ultrastructure, bioenergetic stress, and downstream effects on apoptosis and cellular metabolism. These processes are frequently interrogated in studies of neurodegeneration, myopathies, and cancer-associated metabolic remodeling where mitochondrial structure–function relationships are central.
MINOS1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MINOS1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MINOS1. 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 MINOS1 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 MINOS1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.