Date published: 2026-7-11

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FADD Double Nickase Plasmid (h): sc-400580-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • FADD 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
  • FADD Double Nickase Plasmid (h) and FADD Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FADD. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: FADD Antibody (G-4): sc-271748
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    FADD Double Nickase Plasmid (h)

    sc-400580-NIC
    20 µg
    $410.00

    FADD Double Nickase Plasmid (h2)

    sc-400580-NIC-2
    20 µg
    $410.00

    FADD (Fas-associated protein with death domain) is an essential adaptor that couples activated death receptors such as FAS/CD95 and TNFRSF10 (TRAIL receptors) to initiator caspases, enabling extrinsic apoptosis through death-inducing signaling complex formation. Beyond apoptosis, FADD participates in crosstalk with NF-κB and MAPK pathways and contributes to regulation of necroptosis by modulating RIPK1/RIPK3 signaling balance. Altered FADD expression or signaling has been associated with dysregulated cell survival, aberrant inflammatory responses, and tumorigenesis, making it a common node in studies of immune homeostasis and stress-induced cell death. These functions position FADD as a mechanistic link between receptor signaling, protease activation cascades, and context-dependent outcomes in human cells.

    FADD Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FADD locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FADD. 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 FADD 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 FADD-disrupted clones.

    For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.