Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Oma1 Double Nickase Plasmid (h): sc-402953-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Oma1 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
- Oma1 Double Nickase Plasmid (h) and Oma1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting OMA1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Oma1 Antibody (H-11): sc-515788
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Oma1 Double Nickase Plasmid (h) | sc-402953-NIC | 20 µg | $410.00 | |||
Oma1 Double Nickase Plasmid (h2) | sc-402953-NIC-2 | 20 µg | $410.00 |
Human OMA1 encodes the stress-activated mitochondrial inner membrane metalloprotease Oma1, a key regulator of mitochondrial quality control. Oma1 is rapidly engaged by membrane depolarization and proteotoxic stress to cleave OPA1, shifting mitochondrial dynamics toward fission and coordinating mitophagy, bioenergetic remodeling, and integrated stress signaling. Through this OMA1–OPA1 axis, the protein influences cristae architecture, respiratory chain efficiency, and apoptosis susceptibility. Dysregulation of OMA1-dependent proteostasis and dynamics has been implicated in mitochondrial dysfunction observed across neurodegeneration, cardiometabolic stress, and other disorders linked to impaired mitochondrial homeostasis.
Oma1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the OMA1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within OMA1. 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 OMA1 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 OMA1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.