Date published: 2026-7-10

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CD27L CRISPR/Cas9 KO Plasmid (m): sc-423453

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • CD27L 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 CD27L 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: CD27L Antibody (G-7): sc-365539
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    CD27L CRISPR/Cas9 KO Plasmid (m)

    sc-423453
    20 µg
    $397.00

    Overview

    Cd70 encodes CD27L (CD70), a type II membrane ligand in the TNF superfamily that engages CD27 on T cells, B cells, and NK cells to modulate costimulatory signaling. CD27–CD70 interactions shape adaptive immune activation, supporting lymphocyte expansion, survival, and differentiation through downstream NF-κB and MAPK-linked transcriptional programs. Tight regulation of CD70 expression on activated antigen-presenting cells helps balance immune priming with immune homeostasis. Dysregulated CD70 signaling has been implicated in aberrant inflammatory responses, altered germinal center dynamics, and immune dysregulation relevant to autoimmunity and cancer immunobiology research.

    CD27L CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Cd70 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Cd70 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 Cd70 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 CD27L protein expression.

    This CRISPR knockout system enables efficient generation of Cd70-deficient cell models for investigation of CD27L signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Cd70 exon(s) critical for CD27L 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 Cd70 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by CD27L CRISPR/Cas9 KO Plasmid (m) and CD27L CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Cd70 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by CD27L HDR Plasmid (m) and CD27L HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Cd70 homology arms to support homology-directed repair at defined Cd70 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.