Date published: 2026-7-10

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CD137L CRISPR/Cas9 KO Plasmid (m): sc-423455

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • CD137L 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 CD137L 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: CD137L Antibody (G-10): sc-398933
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    CD137L CRISPR/Cas9 KO Plasmid (m)

    sc-423455
    20 µg
    $397.00

    Overview

    Tnfsf9 encodes CD137L (4-1BBL), a TNF superfamily ligand expressed primarily on antigen-presenting cells that engages CD137 (TNFRSF9) to deliver potent costimulatory cues to T cells and other immune effectors. CD137L–CD137 signaling promotes NF-κB and MAPK pathway activation, supporting T-cell expansion, survival, cytokine production, and the shaping of memory responses, with additional effects on dendritic cell maturation and myeloid cell function. In mouse models, Tnfsf9 activity is implicated in regulation of inflammatory circuits and immune homeostasis, influencing contexts such as autoimmunity, chronic inflammation, and tumor immune surveillance. These roles make CD137L a useful node for dissecting costimulation-dependent immune phenotypes and antigen-driven responses.

    CD137L CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Tnfsf9 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Tnfsf9 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 Tnfsf9 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 CD137L protein expression.

    This CRISPR knockout system enables efficient generation of Tnfsf9-deficient cell models for investigation of CD137L signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Tnfsf9 exon(s) critical for CD137L 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 Tnfsf9 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by CD137L CRISPR/Cas9 KO Plasmid (m) and CD137L CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Tnfsf9 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by CD137L HDR Plasmid (m) and CD137L HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Tnfsf9 homology arms to support homology-directed repair at defined Tnfsf9 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.