Date published: 2026-7-9

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EOMES CRISPR/Cas9 KO Plasmid (m): sc-420182

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • EOMES 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 EOMES 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: EOMES Antibody (1A8): sc-293481
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    EOMES CRISPR/Cas9 KO Plasmid (m)

    sc-420182
    20 µg
    $397.00

    Overview

    Eomes (EOMES) encodes a T-box transcription factor that orchestrates cell fate decisions during mouse development and immune differentiation. EOMES regulates transcriptional programs controlling mesoderm formation, early embryonic patterning, and lineage specification, and it is a key node in pathways that shape cytotoxic lymphocyte maturation and effector function, including NK and CD8+ T cell responses. Through context-dependent interactions with chromatin regulators and cytokine-driven signaling networks, EOMES influences proliferation, migration, and terminal differentiation states. Dysregulated EOMES activity has been implicated in altered immune homeostasis and developmental phenotypes, making it a useful target for mechanistic studies of transcriptional control in development and immunology.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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