C19orf12 Double Nickase Plasmid (h): sc-406640-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- C19orf12 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
- C19orf12 Double Nickase Plasmid (h) and C19orf12 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting C19orf12. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
C19orf12 Double Nickase Plasmid (h) | sc-406640-NIC | 20 µg | $410.00 | |||
C19orf12 Double Nickase Plasmid (h2) | sc-406640-NIC-2 | 20 µg | $410.00 |
C19orf12 encodes a small, mitochondria-associated membrane protein implicated in lipid homeostasis and mitochondrial quality control, with reported roles in oxidative stress responses and membrane remodeling. Its function is linked to mitochondrial metabolism and iron/lipid interplay that influence cellular redox balance and susceptibility to stress-induced damage. Altered C19orf12 activity is associated with neurodegeneration with brain iron accumulation (NBIA), particularly MPAN, highlighting relevance to pathways governing neuronal maintenance, mitochondrial integrity, and iron-handling processes. As a result, C19orf12 is frequently studied in models of mitochondrial dysfunction, lipid metabolism, and neurodegenerative disease mechanisms.
C19orf12 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the C19orf12 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within C19orf12. 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 C19orf12 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 C19orf12-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.