Date published: 2026-7-11

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IP3R-III Double Nickase Plasmid (h): sc-402138-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • IP3R-III 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
  • IP3R-III Double Nickase Plasmid (h) and IP3R-III Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ITPR3. One or both designs may be available
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    IP3R-III Double Nickase Plasmid (h)

    sc-402138-NIC
    20 µg
    $410.00

    IP3R-III Double Nickase Plasmid (h2)

    sc-402138-NIC-2
    20 µg
    $410.00

    Human ITPR3 encodes IP3R-III, an endoplasmic reticulum membrane Ca²⁺ release channel activated by inositol 1,4,5-trisphosphate generated downstream of phospholipase C signaling. By shaping cytosolic and organellar Ca²⁺ dynamics, IP3R-III regulates excitation–secretion coupling, mitochondrial bioenergetics, ER stress responses, and apoptosis through Ca²⁺ transfer at ER–mitochondria contact sites. ITPR3-dependent calcium flux integrates GPCR and receptor tyrosine kinase inputs with transcriptional programs and metabolic adaptation, influencing cell fate decisions. Dysregulated IP3R-III expression or signaling has been associated with altered calcium homeostasis in cancer biology, epithelial physiology, and inflammatory signaling contexts, supporting its use as a mechanistic node in pathway studies.

    IP3R-III Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ITPR3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ITPR3. 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 ITPR3 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 ITPR3-disrupted clones.

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