Date published: 2026-7-11

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NFKBIA/IkB alpha Double Nickase Plasmid (h): sc-400034-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • NFKBIA/IkB alpha 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
  • NFKBIA/IkB alpha Double Nickase Plasmid (h) and NFKBIA/IkB alpha Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting NFKBIA. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: p-NFKBIA/IkB alpha Antibody (B-9): sc-8404
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    NFKBIA/IkB alpha Double Nickase Plasmid (h)

    sc-400034-NIC
    20 µg
    $410.00

    NFKBIA/IkB alpha Double Nickase Plasmid (h2)

    sc-400034-NIC-2
    20 µg
    $410.00

    NFKBIA encodes IκBα, a core inhibitory regulator of canonical NF-κB signaling that binds RELA/p50 complexes and sequesters them in the cytoplasm until IKK-mediated phosphorylation triggers ubiquitination and proteasomal degradation. Through this feedback-controlled mechanism, IκBα modulates stimulus-dependent transcriptional programs governing inflammation, innate and adaptive immunity, cell survival, and stress responses. Dysregulated NFKBIA activity or expression has been linked to aberrant NF-κB pathway activation observed across immune-mediated disorders and multiple cancer contexts, where altered signaling can impact cytokine networks, apoptosis resistance, and microenvironmental signaling. As a central node in TNF, IL-1, TLR, and antigen receptor pathways, NFKBIA is frequently studied to dissect NF-κB dynamics, transcriptional feedback, and pathway cross-talk.

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

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