Date published: 2026-7-11

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IP3R-I CRISPR/Cas9 KO Plasmid (m): sc-421192

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • IP3R-I CRISPR/Cas9 Knockout (KO) Plasmid (m) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
  • gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the IP3R-I genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
  • The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: IP3R-I Antibody (E-8): sc-271197
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    IP3R-I CRISPR/Cas9 KO Plasmid (m)

    sc-421192
    20 µg
    $397.00

    Overview

    Itpr1 encodes inositol 1,4,5-trisphosphate receptor type 1 (IP3R-I), an endoplasmic reticulum Ca²⁺ release channel that converts IP3 generated downstream of PLC-coupled receptors into cytosolic calcium signals. IP3R-I-driven Ca²⁺ transients coordinate synaptic transmission, neuronal excitability, gene expression, and mitochondrial metabolism, and they shape Ca²⁺-dependent processes such as autophagy and apoptosis. In mouse, Itpr1 is highly relevant to neural circuit function, particularly in cerebellar Purkinje neurons, and is commonly studied in the context of motor coordination and neurodegeneration-associated cellular phenotypes. Altered IP3R-I signaling is also linked to broader defects in Ca²⁺ homeostasis that impact ER stress responses and intracellular signaling networks.

    IP3R-I CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Itpr1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Itpr1 together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.

    The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the Itpr1 open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish IP3R-I protein expression.

    This CRISPR knockout system enables efficient generation of Itpr1-deficient cell models for investigation of IP3R-I signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Itpr1 exon(s) critical for IP3R-I function
    • Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
    • GFP reporter for identification of transfected cells
    • Pool of plasmids targeting multiple Itpr1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by IP3R-I CRISPR/Cas9 KO Plasmid (m) and IP3R-I CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Itpr1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by IP3R-I HDR Plasmid (m) and IP3R-I HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Itpr1 homology arms to support homology-directed repair at defined Itpr1 target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.

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