Date published: 2026-7-9

1-800-457-3801

SCBT Portrait Logo
Seach Input

Triadin Double Nickase Plasmid (m): sc-429407-NIC

0.0(0)
Write a reviewAsk a question

Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Triadin Double Nickase Plasmid (m) 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
  • Triadin Double Nickase Plasmid (m) and Triadin Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Trdn. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Triadin Antibody (IIG12): sc-59724
    Gene Editing Promo Banner

    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Triadin Double Nickase Plasmid (m)

    sc-429407-NIC
    20 µg
    $410.00

    Triadin Double Nickase Plasmid (m2)

    sc-429407-NIC-2
    20 µg
    $410.00

    Trdn encodes triadin, a junctional sarcoplasmic reticulum membrane protein that organizes excitation–contraction coupling in striated muscle by linking the ryanodine receptor complex to luminal Ca²⁺-binding proteins such as calsequestrin. In mouse cardiomyocytes and skeletal myofibers, triadin helps tune intracellular Ca²⁺ release and reuptake kinetics that shape contractile force, refractoriness, and Ca²⁺ homeostasis signaling. Through its role in sarcoplasmic reticulum microdomain architecture, triadin influences Ca²⁺-dependent pathways that regulate muscle development, stress responses, and electrophysiological stability. Disruption of TRDN function is associated with inherited arrhythmia phenotypes and myopathic features, making Trdn a relevant target for modeling Ca²⁺ handling defects and sarcoplasmic reticulum remodeling.

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

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