FANCA Double Nickase Plasmid (h): sc-403205-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FANCA 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
- FANCA Double Nickase Plasmid (h) and FANCA Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FANCA. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FANCA Double Nickase Plasmid (h) | sc-403205-NIC | 20 µg | $410.00 | |||
FANCA Double Nickase Plasmid (h2) | sc-403205-NIC-2 | 20 µg | $410.00 |
FANCA encodes a core component of the Fanconi anemia (FA) DNA repair pathway that safeguards genome integrity during replication stress by promoting repair of DNA interstrand crosslinks. FANCA participates in the FA core complex that enables monoubiquitination of FANCD2 and FANCI, coordinating downstream nucleolytic processing, homologous recombination, and replication fork protection. Disruption of FANCA impairs checkpoint control and increases chromosome breakage and micronucleus formation, particularly after exposure to crosslinking damage. Pathogenic variants in FANCA are a major cause of Fanconi anemia and are also relevant to studies of bone marrow failure biology and DNA damage response vulnerabilities in cancer models.
FANCA Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FANCA locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FANCA. 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 FANCA 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 FANCA-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.