Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Factor VII Double Nickase Plasmid (h): sc-402582-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Factor VII 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
- Factor VII Double Nickase Plasmid (h) and Factor VII Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting F7. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Factor VII Antibody (CaFVII-22): sc-101369
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Factor VII Double Nickase Plasmid (h) | sc-402582-NIC | 20 µg | $410.00 | |||
Factor VII Double Nickase Plasmid (h2) | sc-402582-NIC-2 | 20 µg | $410.00 |
Human F7 encodes coagulation factor VII, a vitamin K–dependent serine protease zymogen produced primarily by hepatocytes and secreted into plasma. Upon vascular injury, factor VII binds tissue factor (F3) and is converted to factor VIIa, forming the extrinsic tenase complex that initiates the coagulation cascade through activation of factor X and factor IX, with downstream thrombin generation and fibrin formation. This tissue factor–factor VIIa axis intersects with cell signaling via protease-activated receptors (PARs), linking hemostatic proteolysis to inflammatory and vascular biology pathways. Altered F7 expression or activity is associated with bleeding diatheses and is also studied in the context of thrombosis risk and coagulation–inflammation crosstalk.
Factor VII Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the F7 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within F7. 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 F7 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 F7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.