Date published: 2026-9-10

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TRPV5 CRISPR/Cas9 KO Plasmid (m): sc-431458

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • TRPV5 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 TRPV5 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: TRPV5 Antibody (B-8): sc-398345
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    TRPV5 CRISPR/Cas9 KO Plasmid (m)

    sc-431458
    20 µg
    $397.00

    Overview

    Trpv5 encodes TRPV5, a highly calcium-selective member of the transient receptor potential vanilloid family that functions as an apical epithelial Ca²⁺ entry channel. In mouse kidney distal convoluted tubule and connecting tubule, TRPV5 supports transcellular calcium reabsorption and integrates with calbindin-mediated buffering and basolateral extrusion via NCX1 and PMCA, shaping systemic calcium homeostasis. Channel activity is modulated by intracellular Ca²⁺ feedback, phosphoinositide signaling, pH, and hormonal regulators including vitamin D and PTH, linking TRPV5 to Ca²⁺-dependent signaling and epithelial transport programs. Dysregulation of TRPV5-dependent transport is relevant to studies of hypercalciuria, nephrolithiasis susceptibility, and mineral metabolism phenotypes in mouse models.

    TRPV5 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Trpv5 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Trpv5 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 Trpv5 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 TRPV5 protein expression.

    This CRISPR knockout system enables efficient generation of Trpv5-deficient cell models for investigation of TRPV5 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Trpv5 exon(s) critical for TRPV5 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 Trpv5 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by TRPV5 CRISPR/Cas9 KO Plasmid (m) and TRPV5 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Trpv5 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by TRPV5 HDR Plasmid (m) and TRPV5 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Trpv5 homology arms to support homology-directed repair at defined Trpv5 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.