FANCB Double Nickase Plasmid (h): sc-417439-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FANCB 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
- FANCB Double Nickase Plasmid (h) and FANCB Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FANCB. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FANCB Double Nickase Plasmid (h) | sc-417439-NIC | 20 µg | $410.00 | |||
FANCB Double Nickase Plasmid (h2) | sc-417439-NIC-2 | 20 µg | $410.00 |
FANCB encodes a core component of the Fanconi anemia (FA) nuclear complex that enables monoubiquitination of FANCD2 and FANCI, a pivotal step in the FA DNA interstrand crosslink repair pathway. Through coordination with homologous recombination and replication fork protection factors, FANCB helps maintain genome stability during S phase and under genotoxic stress. Loss-of-function alterations in FANCB are linked to Fanconi anemia and contribute to chromosomal instability phenotypes relevant to cancer biology. FANCB is therefore commonly studied in DNA damage response signaling, replication stress, and pathway epistasis analyses.
FANCB Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FANCB locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FANCB. 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 FANCB 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 FANCB-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.