Date published: 2026-7-11

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FOXP3 CRISPR/Cas9 KO Plasmid (m): sc-422896

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • FOXP3 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 FOXP3 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: FOXP3 Antibody (2A11G9): sc-53876
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    FOXP3 CRISPR/Cas9 KO Plasmid (m)

    sc-422896
    20 µg
    $397.00

    Overview

    Foxp3 encodes FOXP3, a forkhead/winged-helix transcription factor that serves as a master regulator of regulatory T (Treg) cell lineage commitment and suppressive function in mouse. FOXP3 orchestrates transcriptional programs controlling immune tolerance, cytokine homeostasis, and T cell activation thresholds through interactions with factors such as NFAT, RUNX1, and chromatin-modifying complexes. In immune tissues, FOXP3-dependent networks shape peripheral tolerance, limit inflammatory responses, and influence crosstalk between T cells and antigen-presenting cells. Dysregulation of Foxp3 expression or FOXP3 activity is widely used as a mechanistic entry point for studying breakdowns in immune regulation relevant to autoimmunity, allergy, and inflammatory disease models.

    FOXP3 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Foxp3 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Foxp3 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 Foxp3 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 FOXP3 protein expression.

    This CRISPR knockout system enables efficient generation of Foxp3-deficient cell models for investigation of FOXP3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Foxp3 exon(s) critical for FOXP3 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 Foxp3 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by FOXP3 CRISPR/Cas9 KO Plasmid (m) and FOXP3 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Foxp3 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by FOXP3 HDR Plasmid (m) and FOXP3 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Foxp3 homology arms to support homology-directed repair at defined Foxp3 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.