FUNDC1 Double Nickase Plasmid (h): sc-403031-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FUNDC1 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
- FUNDC1 Double Nickase Plasmid (h) and FUNDC1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FUNDC1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FUNDC1 Double Nickase Plasmid (h) | sc-403031-NIC | 20 µg | $410.00 |
FUNDC1 encodes an outer mitochondrial membrane receptor that promotes hypoxia- and stress-induced mitophagy by binding LC3 through its LIR motif and coordinating the turnover of damaged mitochondria. Its activity is regulated by phosphorylation-dependent control of LC3 affinity and intersects with mitochondrial dynamics, bioenergetic homeostasis, and reactive oxygen species signaling. Through these processes, FUNDC1 influences cell survival programs linked to ischemic stress responses, neurodegeneration-associated mitochondrial quality control defects, and metabolic dysregulation. Altered FUNDC1 function has been studied in contexts where perturbed mitophagy contributes to inflammation and tissue injury, making it a useful node for probing mitochondrial stress pathways.
FUNDC1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FUNDC1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FUNDC1. 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 FUNDC1 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 FUNDC1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.