Date published: 2026-7-9

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β-defensin 1 CRISPR/Cas9 KO Plasmid (m): sc-419980

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • β-defensin 1 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 β-defensin 1 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

    β-defensin 1 CRISPR/Cas9 KO Plasmid (m)

    sc-419980
    20 µg
    $397.00

    Overview

    Defb1 encodes mouse β-defensin 1, a small cationic antimicrobial peptide produced by epithelial cells and enriched at barrier surfaces such as the respiratory, gastrointestinal, and urogenital tracts. β-defensin 1 contributes to innate immune defense through direct microbicidal activity and by shaping mucosal microbiome composition, while also functioning as an immunomodulator that can influence leukocyte recruitment and cytokine signaling. Its expression is linked to epithelial differentiation programs and inflammatory responses, connecting Defb1 to processes that regulate barrier integrity and host–pathogen interactions. Altered defensin expression has been associated with susceptibility to infection and inflammatory disease phenotypes in experimental models, supporting its relevance for studies of mucosal immunology and epithelial homeostasis.

    β-defensin 1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Defb1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Defb1 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 Defb1 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 β-defensin 1 protein expression.

    This CRISPR knockout system enables efficient generation of Defb1-deficient cell models for investigation of β-defensin 1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Defb1 exon(s) critical for β-defensin 1 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 Defb1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by β-defensin 1 CRISPR/Cas9 KO Plasmid (m) and β-defensin 1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Defb1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by β-defensin 1 HDR Plasmid (m) and β-defensin 1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Defb1 homology arms to support homology-directed repair at defined Defb1 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.