FOXM1 Double Nickase Plasmid (h): sc-416676-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FOXM1 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
- FOXM1 Double Nickase Plasmid (h) and FOXM1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FOXM1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: FOXM1 Antibody (G-5): sc-376471
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FOXM1 Double Nickase Plasmid (h) | sc-416676-NIC | 20 µg | $410.00 | |||
FOXM1 Double Nickase Plasmid (h2) | sc-416676-NIC-2 | 20 µg | $410.00 |
FOXM1 is a forkhead box transcription factor that coordinates cell-cycle progression by regulating genes required for G1/S transition, DNA replication, and G2/M mitotic entry. It integrates signaling from pathways such as CDK–RB/E2F and PLK1- and Aurora kinase–associated mitotic networks to maintain proliferative competence and genomic stability. FOXM1 also modulates DNA damage responses and oxidative stress programs, linking checkpoint control with replication stress tolerance. Dysregulated FOXM1 expression and activity are frequently associated with uncontrolled proliferation, chromosomal instability, and altered tumor cell biology, making it a widely studied node in cancer and cell-cycle research.
FOXM1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FOXM1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FOXM1. 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 FOXM1 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 FOXM1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.