TLR6 CRISPR/Cas9 KO Plasmid (m): sc-423420
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TLR6 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 TLR6 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
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TLR6 CRISPR/Cas9 KO Plasmid (m) | sc-423420 | 20 µg | $397.00 |
Overview
Tlr6 encodes toll-like receptor 6 (TLR6), a pattern-recognition receptor that forms functional heterodimers with TLR2 to detect microbial lipopeptides at the cell surface and initiate innate immune signaling. Upon ligand binding, TLR6 engages adaptor proteins such as MYD88 to activate IRAK–TRAF6 signaling, driving NF-κB and MAPK pathway activation and induction of inflammatory cytokines and chemokines. In mouse myeloid and epithelial compartments, TLR6 contributes to shaping antimicrobial responses and modulating crosstalk between innate and adaptive immunity. Dysregulated TLR6-dependent signaling has been implicated in inflammatory pathobiology, including altered responses in infection, airway inflammation, and metabolic inflammation models.
TLR6 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Tlr6 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Tlr6 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 Tlr6 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 TLR6 protein expression.
This CRISPR knockout system enables efficient generation of Tlr6-deficient cell models for investigation of TLR6 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Tlr6 exon(s) critical for TLR6 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 Tlr6 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TLR6 CRISPR/Cas9 KO Plasmid (m) and TLR6 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Tlr6 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TLR6 HDR Plasmid (m) and TLR6 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Tlr6 homology arms to support homology-directed repair at defined Tlr6 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.