Date published: 2026-8-1

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ETAR Double Nickase Plasmid (h): sc-401000-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • ETAR 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
  • ETAR Double Nickase Plasmid (h) and ETAR Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting EDNRA. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ETAR Antibody (D-2): sc-518060
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    ETAR Double Nickase Plasmid (h)

    sc-401000-NIC
    20 µg
    $410.00

    ETAR Double Nickase Plasmid (h2)

    sc-401000-NIC-2
    20 µg
    $410.00

    Endothelin receptor type A (ETAR), encoded by the human EDNRA gene, is a G protein–coupled receptor that binds endothelin-1 to regulate vascular smooth muscle contraction, cell proliferation, and calcium-dependent signaling. ETAR primarily couples to Gq/11 to activate phospholipase C, generate IP3/DAG, and engage downstream MAPK and Rho/ROCK pathways, integrating signals that shape vasomotor tone and tissue remodeling. EDNRA-driven signaling influences endothelial–smooth muscle crosstalk and contributes to angiogenic and inflammatory programs in diverse cellular contexts. Dysregulated ETAR activity has been associated with cardiopulmonary vascular dysfunction, fibrotic remodeling, and tumor microenvironment processes, making EDNRA a useful target for mechanistic studies of receptor signaling networks.

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

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