
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-28B CRISPR Activation Plasmid (h) | sc-406651-ACT | 20 µg | $397.00 | |||
IL-28B CRISPR Activation Plasmid (h2) | sc-406651-ACT-2 | 20 µg | $397.00 |
Human IFNL3 encodes interferon lambda 3 (IL-28B), a type III interferon that signals through the IFNLR1/IL10RB receptor complex to activate JAK–STAT pathways and induce interferon-stimulated genes that shape intrinsic antiviral defenses at epithelial and barrier surfaces. IL-28B-driven transcriptional programs regulate innate immune sensing, antigen presentation, and inflammatory tone, intersecting with STAT1/STAT2–IRF9 (ISGF3) and IRF-mediated networks. Variation in IFNL3 expression has been linked to differential host responses to viral infection and immune-mediated inflammation, making it a useful node for studying cytokine crosstalk and interferon pathway regulation. In cell models, modulating IFNL3 helps interrogate epithelial immune signaling, viral restriction mechanisms, and downstream ISG dynamics without directly altering pathogen components.
IL-28B CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous IFNL3 expression without altering the underlying DNA sequence.
IL-28B CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the IFNL3 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 IFNL3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IL-28B expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native IFNL3 locus and enabling the study of IL-28B-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IL-28B pathway restoration in tumor cells with silenced or reduced IFNL3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.