Date published: 2026-8-28

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LTβR Double Nickase Plasmid (h): sc-402774-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • LTβR 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
  • LTβR Double Nickase Plasmid (h) and LTβR Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting LTBR. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: LTβR Antibody (H-2): sc-398929
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    LTβR Double Nickase Plasmid (h)

    sc-402774-NIC
    20 µg
    $410.00

    LTβR Double Nickase Plasmid (h2)

    sc-402774-NIC-2
    20 µg
    $410.00

    Human LTBR encodes lymphotoxin beta receptor (LTβR), a TNF receptor superfamily member that binds lymphotoxin-α1β2 and LIGHT to coordinate stromal–immune crosstalk. LTβR signaling activates canonical and non-canonical NF-κB pathways through TRAF adaptors, shaping chemokine production, lymphoid organogenesis, and maintenance of lymphoid tissue architecture. In immune cells and stromal compartments, LTβR regulates inflammatory gene programs, antigen-presenting microenvironments, and barrier-associated responses. Dysregulated LTβR activity has been implicated in chronic inflammation and autoimmunity, and it is frequently studied in tumor microenvironment remodeling and immune evasion mechanisms.

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

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