Date published: 2026-7-8

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TREM-1 Double Nickase Plasmid (h): sc-417344-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • TREM-1 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
  • TREM-1 Double Nickase Plasmid (h) and TREM-1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TREM1. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TREM-1 Antibody (2E2): sc-293450
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    TREM-1 Double Nickase Plasmid (h)

    sc-417344-NIC
    20 µg
    $410.00

    TREM-1 Double Nickase Plasmid (h2)

    sc-417344-NIC-2
    20 µg
    $410.00

    Human TREM1 encodes the triggering receptor expressed on myeloid cells 1 (TREM-1), an immunoglobulin superfamily receptor enriched on neutrophils and monocytes/macrophages that amplifies innate inflammatory responses. Through association with the adaptor TYROBP/DAP12, TREM-1 signaling activates SYK-dependent pathways, converging on MAPK and NF-κB transcriptional programs that enhance cytokine and chemokine production and promote myeloid cell activation. TREM-1 is widely studied in the context of inflammation-driven tissue injury and dysregulated myeloid responses, including sepsis, acute lung injury, inflammatory bowel disease, and tumor-associated inflammation. These features make TREM1 a useful target for interrogating myeloid signaling networks, inflammatory crosstalk, and pathway-dependent transcriptional outputs.

    TREM-1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TREM1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TREM1. 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 TREM1 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 TREM1-disrupted clones.

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