Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
TLR9 CRISPR Activation Plasmid (h): sc-400600-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TLR9 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- TLR9 CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by TLR9 CRISPR Activation Plasmid (h) and TLR9 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the TLR9 transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TLR9 Antibody (5G5): sc-47723
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TLR9 CRISPR Activation Plasmid (h) | sc-400600-ACT | 20 µg | $397.00 | |||
TLR9 CRISPR Activation Plasmid (h2) | sc-400600-ACT-2 | 20 µg | $397.00 |
TLR9 encodes Toll-like receptor 9, an endosomal pattern-recognition receptor that detects unmethylated CpG motifs in microbial and mitochondrial DNA to initiate innate immune signaling. Upon ligand engagement, TLR9 signals primarily through MYD88 to activate IRAK/TRAF6-dependent cascades that converge on NF-κB and IRF transcriptional programs, promoting inflammatory cytokine and type I interferon responses. This pathway shapes dendritic cell maturation, B cell activation, and antimicrobial defense, and its dysregulation has been implicated in chronic inflammation and autoimmune-associated immune activation. Human TLR9 is therefore widely studied in nucleic-acid sensing, endosomal trafficking, and PRR cross-talk networks relevant to immune homeostasis.
TLR9 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TLR9 expression without altering the underlying DNA sequence.
TLR9 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TLR9 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the TLR9 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TLR9 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TLR9 locus and enabling the study of TLR9-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TLR9 pathway restoration in tumor cells with silenced or reduced TLR9 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.