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.
TLR2 CRISPR Activation Plasmid (h): sc-400267-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TLR2 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- TLR2 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 TLR2 CRISPR Activation Plasmid (h) and TLR2 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the TLR2 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: TLR2 Antibody (TL2.1): sc-21759
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TLR2 CRISPR Activation Plasmid (h) | sc-400267-ACT | 20 µg | $397.00 | |||
TLR2 CRISPR Activation Plasmid (h2) | sc-400267-ACT-2 | 20 µg | $397.00 |
Human TLR2 encodes Toll-like receptor 2, a pattern-recognition receptor that detects bacterial lipoproteins and other microbial components in cooperation with heterodimer partners such as TLR1 and TLR6. Upon ligand engagement, TLR2 signals primarily through MYD88-dependent pathways to activate IRAK–TRAF6 cascades, driving NF-κB and MAPK signaling and induction of pro-inflammatory cytokines and chemokines. TLR2 activity shapes innate immune activation, dendritic cell maturation, and crosstalk with adaptive immunity, with downstream effects on interferon and inflammasome-associated programs in a context-dependent manner. Dysregulated TLR2 signaling has been implicated in chronic inflammatory conditions, infection-associated immunopathology, and tumor-associated inflammation, making it a useful target for mechanistic studies of immune regulation.
TLR2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TLR2 expression without altering the underlying DNA sequence.
TLR2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TLR2 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 TLR2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TLR2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TLR2 locus and enabling the study of TLR2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TLR2 pathway restoration in tumor cells with silenced or reduced TLR2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.