
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-23R CRISPR Activation Plasmid (h) | sc-403591-ACT | 20 µg | $397.00 |
Human IL23R encodes the IL-23 receptor subunit IL-23R, a key component of the IL-23 receptor complex that couples IL-23 sensing to intracellular JAK/STAT signaling, most prominently STAT3-driven transcriptional programs. IL-23R expression on activated T cells and innate lymphoid populations supports Th17-associated cytokine networks and coordinates epithelial barrier and mucosal immune responses. Through regulation of effector cytokines and inflammatory gene expression, IL23R contributes to immune cell differentiation, trafficking, and tissue inflammation. Genetic and expression studies implicate IL23R pathway perturbation in immune-mediated inflammatory diseases, making it a widely used node for mechanistic studies of cytokine signaling.
IL-23R CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous IL23R expression without altering the underlying DNA sequence.
IL-23R CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the IL23R 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 IL23R transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IL-23R expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native IL23R locus and enabling the study of IL-23R-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IL-23R pathway restoration in tumor cells with silenced or reduced IL23R expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.