
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-1RII CRISPR Activation Plasmid (m) | sc-421099-ACT | 20 µg | $397.00 |
Mouse Il1r2 encodes interleukin-1 receptor type II (IL-1RII), a high-affinity decoy receptor that binds IL-1α and IL-1β to limit productive signaling through IL-1R1. By sequestering ligands and modulating receptor complex availability, IL-1RII shapes innate immune activation and inflammatory transcriptional programs linked to NF-κB and MAPK pathway outputs. IL-1RII expression is dynamically regulated in myeloid and stromal compartments, influencing cytokine networks, leukocyte recruitment, and resolution of inflammation. Dysregulated IL-1 axis control, including altered IL-1RII levels, has been associated with chronic inflammatory phenotypes and immune-mediated pathology in experimental mouse disease models.
IL-1RII CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Il1r2 expression without altering the underlying DNA sequence.
IL-1RII CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Il1r2 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 Il1r2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IL-1RII expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Il1r2 locus and enabling the study of IL-1RII-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IL-1RII pathway restoration in tumor cells with silenced or reduced Il1r2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.