
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-18Rβ CRISPR Activation Plasmid (h) | sc-411213-ACT | 20 µg | $397.00 |
IL18RAP encodes IL-18 receptor accessory protein (IL-18Rβ), a coreceptor that pairs with IL18R1 to form the functional IL-18 receptor complex on immune and stromal cells. Upon IL-18 binding, this heterodimer engages MyD88-dependent signaling to activate IRAK/TRAF6 cascades, driving NF-κB and MAPK pathway output and shaping IFN-γ–skewed inflammatory programs. IL-18Rβ activity contributes to regulation of innate and adaptive immune crosstalk, including NK- and T-cell effector responses and cytokine network amplification. Altered IL18RAP expression or signaling has been linked to immune-mediated pathology and inflammatory disease contexts where dysregulated IL-18 axis signaling is implicated.
IL-18Rβ CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous IL18RAP expression without altering the underlying DNA sequence.
IL-18Rβ CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the IL18RAP 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 IL18RAP transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IL-18Rβ expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native IL18RAP locus and enabling the study of IL-18Rβ-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IL-18Rβ pathway restoration in tumor cells with silenced or reduced IL18RAP expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.