TLR7 CRISPR/Cas9 KO Plasmid (m): sc-431302
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TLR7 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 TLR7 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 | |
TLR7 CRISPR/Cas9 KO Plasmid (m) | sc-431302 | 20 µg | $397.00 |
Overview
Tlr7 encodes Toll-like receptor 7 (TLR7), an endosomal pattern-recognition receptor that detects single-stranded RNA and synthetic imidazoquinoline ligands to initiate innate immune signaling. Upon activation, TLR7 couples to MYD88 and engages IRAK–TRAF6 signaling to drive NF-κB and IRF7-dependent transcription of type I interferons and proinflammatory cytokines, shaping antiviral defenses and B cell responses. In mice, TLR7 activity influences dendritic cell activation, germinal center dynamics, and cytokine milieus that coordinate adaptive immunity. Dysregulated TLR7 signaling has been implicated in inflammatory and autoimmune phenotypes and is frequently studied in models of systemic immune activation and pathogen sensing.
TLR7 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Tlr7 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Tlr7 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 Tlr7 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 TLR7 protein expression.
This CRISPR knockout system enables efficient generation of Tlr7-deficient cell models for investigation of TLR7 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Tlr7 exon(s) critical for TLR7 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 Tlr7 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TLR7 CRISPR/Cas9 KO Plasmid (m) and TLR7 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Tlr7 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TLR7 HDR Plasmid (m) and TLR7 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Tlr7 homology arms to support homology-directed repair at defined Tlr7 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.