FLAD1 Double Nickase Plasmid (m): sc-435691-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FLAD1 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
- FLAD1 Double Nickase Plasmid (m) and FLAD1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Flad1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: FLAD1 Antibody (G-4): sc-376819
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FLAD1 Double Nickase Plasmid (m) | sc-435691-NIC | 20 µg | $410.00 |
Flad1 encodes flavin adenine dinucleotide synthetase 1 (FLAD1), a key enzyme that converts FMN to FAD, thereby controlling the cellular pool of this essential redox cofactor. Through regulating FAD-dependent oxidoreductases, FLAD1 supports mitochondrial and peroxisomal metabolism, oxidative phosphorylation, and broader flavoprotein-mediated pathways that influence reactive oxygen species homeostasis. Altered flavin cofactor biosynthesis is linked to defects in energy metabolism and cellular stress responses, making Flad1 a relevant node for studying metabolic vulnerability and redox imbalance. In mouse systems, perturbing Flad1 provides a tractable approach to interrogate cofactor-dependent signaling and enzyme networks across tissues.
FLAD1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Flad1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Flad1. 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 Flad1 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 Flad1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.