RARS2 Double Nickase Plasmid (h): sc-412751-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RARS2 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
- RARS2 Double Nickase Plasmid (h) and RARS2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RARS2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RARS2 Double Nickase Plasmid (h) | sc-412751-NIC | 20 µg | $410.00 | |||
RARS2 Double Nickase Plasmid (h2) | sc-412751-NIC-2 | 20 µg | $410.00 |
RARS2 encodes the mitochondrial arginyl-tRNA synthetase, an essential enzyme that ligates arginine to its cognate tRNA to support mitochondrial translation and oxidative phosphorylation. By sustaining synthesis of mitochondrially encoded respiratory chain subunits, RARS2 links aminoacyl-tRNA charging to electron transport chain assembly, ATP production, and mitochondrial stress responses. Altered RARS2 function has been associated with mitochondrial disease phenotypes featuring impaired energy metabolism and neurodevelopmental involvement, making it a relevant target for studying genotype–mitochondrial function relationships. Its activity intersects with pathways governing mitochondrial ribosome function, proteostasis, and integrated stress signaling.
RARS2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RARS2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RARS2. 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 RARS2 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 RARS2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.