
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-28R CRISPR Activation Plasmid (h) | sc-402530-ACT | 20 µg | $397.00 |
IFNLR1 encodes the interferon lambda receptor 1 (IL-28Rα), the ligand-binding subunit of the type III interferon receptor complex that partners with IL10RB to mediate responses to IFN-λ family cytokines. Receptor engagement activates JAK/STAT signaling, driving STAT1/STAT2/IRF9-dependent transcription of interferon-stimulated genes that shape epithelial barrier antiviral defenses and mucosal immunity. IFNLR1 activity influences innate immune programming, antigen presentation, and inflammatory tone in epithelial-rich tissues, linking receptor expression to variation in antiviral restriction and immune-mediated pathology. Dysregulated IFN-λ/IFNLR signaling has been studied in the context of respiratory and gastrointestinal viral susceptibility, chronic inflammation, and tumor-immune interactions.
IL-28R CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous IFNLR1 expression without altering the underlying DNA sequence.
IL-28R CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the IFNLR1 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 IFNLR1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IL-28R expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native IFNLR1 locus and enabling the study of IL-28R-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IL-28R pathway restoration in tumor cells with silenced or reduced IFNLR1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.