FANCD2 Double Nickase Plasmid (m): sc-431756-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FANCD2 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
- FANCD2 Double Nickase Plasmid (m) and FANCD2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Fancd2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FANCD2 Double Nickase Plasmid (m) | sc-431756-NIC | 20 µg | $410.00 | |||
FANCD2 Double Nickase Plasmid (m2) | sc-431756-NIC-2 | 20 µg | $410.00 |
Fancd2 encodes FANCD2, a central effector of the Fanconi anemia (FA) DNA interstrand crosslink repair pathway that protects genome stability during replication stress. Upon DNA damage, FANCD2 is monoubiquitinated with FANCI and recruited to stalled replication forks, coordinating nucleolytic processing, homologous recombination, and interactions with BRCA-associated repair factors. This activity supports S-phase checkpoint control, limits chromosomal breakage, and preserves replication fork integrity. Disruption of FANCD2-dependent repair is linked to Fanconi anemia biology and hypersensitivity to crosslinking agents, making Fancd2 a key locus for studying replication-coupled DNA repair and genome maintenance in mouse models.
FANCD2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Fancd2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Fancd2. 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 Fancd2 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 Fancd2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.