Fumarylacetoacetase Double Nickase Plasmid (h): sc-402478-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Fumarylacetoacetase 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
- Fumarylacetoacetase Double Nickase Plasmid (h) and Fumarylacetoacetase Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FAH. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Fumarylacetoacetase Double Nickase Plasmid (h) | sc-402478-NIC | 20 µg | $410.00 | |||
Fumarylacetoacetase Double Nickase Plasmid (h2) | sc-402478-NIC-2 | 20 µg | $410.00 |
FAH encodes fumarylacetoacetase, a cytosolic enzyme that catalyzes the terminal step of tyrosine catabolism by converting fumarylacetoacetate to fumarate and acetoacetate, linking amino acid degradation to central carbon metabolism. By preventing accumulation of reactive intermediates such as fumarylacetoacetate and succinylacetone, FAH supports redox homeostasis and limits protein and DNA damage in hepatocytes. Disruption of FAH perturbs tyrosine degradation flux and downstream metabolic signaling, providing a tractable model for studying metabolic stress responses. Genetic deficiency of FAH is associated with hereditary tyrosinemia type I, a liver-centered metabolic disorder that is widely used in experimental systems to investigate hepatotoxic metabolite biology.
Fumarylacetoacetase Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FAH locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FAH. 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 FAH 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 FAH-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.