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.
TLR7 CRISPR Activation Plasmid (h): sc-401189-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TLR7 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- TLR7 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 TLR7 CRISPR Activation Plasmid (h) and TLR7 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the TLR7 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: TLR7 Antibody (C-1): sc-518178
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TLR7 CRISPR Activation Plasmid (h) | sc-401189-ACT | 20 µg | $397.00 | |||
TLR7 CRISPR Activation Plasmid (h2) | sc-401189-ACT-2 | 20 µg | $397.00 |
TLR7 encodes Toll-like receptor 7, an endosomal pattern-recognition receptor that detects uridine-rich single-stranded RNA and synthetic imidazoquinoline ligands, initiating innate antiviral immune signaling. Upon activation, TLR7 signals through MYD88 to engage IRAK kinases and TRAF6, driving NF-κB and IRF7-dependent transcriptional programs that induce type I interferons and proinflammatory cytokines. This pathway shapes dendritic cell and B cell activation, influences adaptive immune priming, and modulates inflammatory set points in mucosal and systemic immunity. Dysregulated TLR7 activity and gene dosage effects have been linked to aberrant interferon signaling and immune dysfunction observed across infection, autoimmunity, and inflammatory disease biology.
TLR7 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TLR7 expression without altering the underlying DNA sequence.
TLR7 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TLR7 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 TLR7 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TLR7 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TLR7 locus and enabling the study of TLR7-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TLR7 pathway restoration in tumor cells with silenced or reduced TLR7 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.