Date published: 2026-8-11

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claudin-11 CRISPR/Cas9 KO Plasmid (h): sc-401859

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • claudin-11 CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 claudin-11 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: claudin-11 Antibody (D-8): sc-271232
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    claudin-11 CRISPR/Cas9 KO Plasmid (h)

    sc-401859
    20 µg
    $397.00

    Overview

    CLDN11 encodes claudin-11, a tetra-spanning tight junction protein that forms paracellular barriers and regulates selective permeability in specialized epithelia. Claudin-11 is a key component of tight junction strand architecture in myelinating glia and testicular Sertoli cell junctions, supporting cell polarity and tissue compartmentalization. Through tight junction assembly and barrier maintenance processes, CLDN11 influences epithelial integrity, ionic homeostasis, and cell–cell adhesion signaling. Altered CLDN11 expression or junctional organization is studied in contexts of barrier dysfunction and dysregulated differentiation, with relevance to nervous system myelination biology and reproductive tissue homeostasis.

    claudin-11 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CLDN11 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CLDN11 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 CLDN11 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 claudin-11 protein expression.

    This CRISPR knockout system enables efficient generation of CLDN11-deficient cell models for investigation of claudin-11 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting CLDN11 exon(s) critical for claudin-11 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 CLDN11 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by claudin-11 CRISPR/Cas9 KO Plasmid (h) and claudin-11 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CLDN11 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by claudin-11 HDR Plasmid (h) and claudin-11 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CLDN11 homology arms to support homology-directed repair at defined CLDN11 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.