Parkin Double Nickase Plasmid (m): sc-424514-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Parkin Double Nickase Plasmid (m) 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
- Parkin Double Nickase Plasmid (m) and Parkin Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Park2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Parkin Antibody (PRK8): sc-32282
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Parkin Double Nickase Plasmid (m) | sc-424514-NIC | 20 µg | $410.00 |
Mouse Park2 encodes the E3 ubiquitin ligase Parkin, a central regulator of mitochondrial quality control that collaborates with PINK1 to label damaged mitochondria for ubiquitin-dependent mitophagy. Parkin-mediated ubiquitination of outer mitochondrial membrane proteins shapes proteasomal turnover, mitochondrial dynamics, and stress-responsive signaling that influences bioenergetic homeostasis. Through these functions, Park2 is broadly used to study pathways linking oxidative stress, mitochondrial dysfunction, and proteostasis in neuronal and non-neuronal systems. Dysregulation of Parkin activity is strongly associated with mechanisms relevant to neurodegeneration, particularly processes implicated in Parkinsonian phenotypes.
Parkin Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Park2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Park2. 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 Park2 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 Park2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.