Date published: 2026-7-5

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SR-1D Double Nickase Plasmid (h): sc-404213-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • SR-1D 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
  • SR-1D Double Nickase Plasmid (h) and SR-1D Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HTR1D. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: SR-1D Antibody (H-4): sc-398809
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    SR-1D Double Nickase Plasmid (h)

    sc-404213-NIC
    20 µg
    $410.00

    SR-1D Double Nickase Plasmid (h2)

    sc-404213-NIC-2
    20 µg
    $410.00

    HTR1D encodes the human serotonin (5-hydroxytryptamine) receptor 1D (SR-1D), a Gi/o-coupled GPCR that dampens adenylate cyclase activity and reduces intracellular cAMP to modulate neuronal excitability and synaptic neurotransmitter release. SR-1D signaling influences MAPK/ERK and ion channel regulation downstream of serotonergic tone, shaping presynaptic control of monoamine transmission in central and peripheral nervous systems. The receptor is studied in pathways governing neurovascular regulation and nociceptive processing, and altered serotonergic GPCR signaling has been associated with neurological disease mechanisms including migraine biology and related headache phenotypes. HTR1D perturbation is also used to probe GPCR desensitization, β-arrestin-mediated trafficking, and circuit-level regulation of serotonin-responsive networks.

    SR-1D Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HTR1D locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HTR1D. 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 HTR1D 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 HTR1D-disrupted clones.

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