FASTKD2 Double Nickase Plasmid (h): sc-417574-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FASTKD2 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
- FASTKD2 Double Nickase Plasmid (h) and FASTKD2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FASTKD2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FASTKD2 Double Nickase Plasmid (h) | sc-417574-NIC | 20 µg | $410.00 |
FASTKD2 (FAST kinase domains 2) encodes a mitochondrial RNA-binding protein that localizes to the matrix and supports post-transcriptional regulation of mitochondrial gene expression. FASTKD2 contributes to maturation, stability, and turnover of mitochondrial RNAs, thereby influencing oxidative phosphorylation and respiratory chain assembly. Through its role in mitochondrial RNA metabolism and proteostasis, FASTKD2 impacts cellular energy homeostasis, stress responses, and apoptosis signaling. Genetic disruption or dysfunction of FASTKD2 has been linked to mitochondrial encephalomyopathy and neurodevelopmental phenotypes, making it a relevant target for investigating mitochondrial disease mechanisms.
FASTKD2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FASTKD2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FASTKD2. 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 FASTKD2 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 FASTKD2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.