Date published: 2026-8-13

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Tenascin-C CRISPR/Cas9 KO Plasmid (m): sc-423430

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Tenascin-C 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 Tenascin-C 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
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Tenascin-C CRISPR/Cas9 KO Plasmid (m)

    sc-423430
    20 µg
    $397.00

    Overview

    Tnc encodes the extracellular matrix glycoprotein Tenascin-C, a highly regulated matricellular protein that modulates cell–matrix interactions during development, tissue remodeling, and inflammation. Tenascin-C influences adhesion and migration by interacting with integrins, fibronectin, and proteoglycans, and it tunes mechanotransduction and growth factor signaling within the stromal niche. It is commonly induced by injury-associated cues and participates in processes such as epithelial–mesenchymal transitions, angiogenic remodeling, and leukocyte recruitment. Dysregulated Tenascin-C expression has been linked to fibrosis, chronic inflammatory microenvironments, and tumor-associated stromal remodeling, making Tnc a useful target for studying extracellular matrix–driven signaling programs.

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

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

    Key Features

    • sgRNAs targeting Tnc exon(s) critical for Tenascin-C 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 Tnc genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

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