Date published: 2026-7-13

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TLR1 CRISPR/Cas9 KO Plasmid (m2): sc-423418-KO-2

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • TLR1 CRISPR/Cas9 Knockout (KO) Plasmid (m2) 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 TLR1 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: TLR1 Antibody (H-8): sc-514399
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    TLR1 CRISPR/Cas9 KO Plasmid (m2)

    sc-423418-KO-2
    20 µg
    $397.00

    Overview

    Tlr1 encodes the mouse Toll-like receptor 1 (TLR1), a pattern-recognition receptor that forms a functional heterodimer with TLR2 to detect triacylated bacterial lipopeptides at the cell surface. Ligand engagement triggers MyD88-dependent signaling and activation of NF-κB and MAPK cascades, promoting transcription of proinflammatory cytokines and chemokines that shape innate and downstream adaptive immune responses. TLR1 activity influences dendritic cell and macrophage activation, barrier immunity, and crosstalk with microbial products within the microbiome. Dysregulated TLR1/TLR2 signaling has been associated with inflammatory phenotypes and altered host defense in infection and immune-mediated disease models.

    TLR1 CRISPR/Cas9 KO Plasmid (m2) is a pool of plasmids designed for targeted disruption of the Tlr1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Tlr1 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 Tlr1 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 TLR1 protein expression.

    This CRISPR knockout system enables efficient generation of Tlr1-deficient cell models for investigation of TLR1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Tlr1 exon(s) critical for TLR1 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 Tlr1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by TLR1 CRISPR/Cas9 KO Plasmid (m) and TLR1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Tlr1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by TLR1 HDR Plasmid (m) and TLR1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Tlr1 homology arms to support homology-directed repair at defined Tlr1 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.