TRIL CRISPR/Cas9 KO Plasmid (h): sc-406056
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRIL CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 TRIL 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 | |
TRIL CRISPR/Cas9 KO Plasmid (h) | sc-406056 | 20 µg | $397.00 |
Overview
TRIL (TLR4 interactor with leucine-rich repeats) is a transmembrane accessory protein that modulates innate immune signaling by facilitating Toll-like receptor 4–dependent responses, particularly in microglia and other myeloid-lineage contexts. Through interactions that support receptor trafficking and ligand responsiveness, TRIL influences downstream MyD88- and TRIF-linked pathways leading to NF-κB and IRF transcriptional programs. Its activity contributes to regulation of cytokine and interferon outputs, shaping neuroinflammatory and inflammatory signaling networks. Dysregulated TRIL-associated signaling has been studied in the context of inflammatory and neuroinflammatory mechanisms relevant to disorders where TLR4-driven responses are implicated.
TRIL CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TRIL gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TRIL 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 TRIL 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 TRIL protein expression.
This CRISPR knockout system enables efficient generation of TRIL-deficient cell models for investigation of TRIL signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TRIL exon(s) critical for TRIL 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 TRIL genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TRIL CRISPR/Cas9 KO Plasmid (h) and TRIL CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TRIL locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TRIL HDR Plasmid (h) and TRIL HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TRIL homology arms to support homology-directed repair at defined TRIL 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.