Date published: 2026-10-7

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Keratin 6B CRISPR/Cas9 KO Plasmid (m): sc-421355

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Keratin 6B 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 Keratin 6B 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

    Keratin 6B CRISPR/Cas9 KO Plasmid (m)

    sc-421355
    20 µg
    $397.00

    Overview

    Krt6b encodes keratin 6B, a type II intermediate filament protein that pairs with type I keratins to build the cytoskeletal network of stratified epithelia. Keratin 6B supports mechanical resilience, epithelial remodeling, and stress-induced programs that accompany wound repair and hyperproliferative states, coordinating with differentiation and cytoskeletal organization processes. In mouse skin and related appendages, Krt6b expression is induced during injury and inflammation, linking keratin filament dynamics to barrier function and tissue homeostasis. Dysregulation of keratin networks is associated with epithelial fragility and aberrant keratinization phenotypes, making Krt6b a useful node for studying keratin-dependent stress responses.

    Keratin 6B CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Krt6b gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Krt6b 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 Krt6b 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 Keratin 6B protein expression.

    This CRISPR knockout system enables efficient generation of Krt6b-deficient cell models for investigation of Keratin 6B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Krt6b exon(s) critical for Keratin 6B 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 Krt6b genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by Keratin 6B CRISPR/Cas9 KO Plasmid (m) and Keratin 6B CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Krt6b locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by Keratin 6B HDR Plasmid (m) and Keratin 6B HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Krt6b homology arms to support homology-directed repair at defined Krt6b 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.