IL-18R CRISPR Activation Plasmid (h): sc-405214-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IL-18R CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- IL-18R 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 IL-18R CRISPR Activation Plasmid (h) and IL-18R CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the IL18R1 transcriptional start site. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-18R CRISPR Activation Plasmid (h) | sc-405214-ACT | 20 µg | $397.00 | |||
IL-18R CRISPR Activation Plasmid (h2) | sc-405214-ACT-2 | 20 µg | $397.00 |
IL18R1 encodes the IL-18 receptor alpha chain (IL-18R), a cell-surface receptor that forms a signaling complex with IL18RAP to mediate responsiveness to the proinflammatory cytokine IL-18. Ligand engagement promotes MyD88-dependent signaling with downstream activation of NF-κB and MAPK pathways, coordinating transcriptional programs that shape Th1 polarization, IFN-γ production, and innate immune activation. IL18R1 expression and signaling are relevant to inflammatory and autoimmune mechanisms, as well as immune regulation within infection and tumor microenvironments. As a result, IL18R is commonly studied in cytokine networks that govern immune cell activation, chemotaxis, and tissue inflammation.
IL-18R CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous IL18R1 expression without altering the underlying DNA sequence.
IL-18R CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the IL18R1 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 IL18R1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IL-18R expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native IL18R1 locus and enabling the study of IL-18R-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IL-18R pathway restoration in tumor cells with silenced or reduced IL18R1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.