
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-28R Lentiviral Activation Particles (h) | sc-402530-LAC | 200 µl | $455.00 |
IFNLR1 encodes interferon lambda receptor 1 (IL-28R), a type II cytokine receptor chain that heterodimerizes with IL10RB to form the functional receptor for type III interferons (IFN-λ/IL-28/IL-29). Ligand engagement initiates JAK–STAT signaling, leading to phosphorylation of STAT1/STAT2, assembly of the ISGF3 complex, and induction of interferon-stimulated genes that shape epithelial and barrier-cell antiviral programs. IL-28R expression is enriched in epithelial tissues and select immune subsets, linking IFNLR1 activity to mucosal immunity, inflammatory signaling, and innate immune regulation. Dysregulated IFNLR1 pathway activity has been studied in the context of viral susceptibility, chronic inflammation, and interferon-driven gene expression signatures relevant to immunopathology.
IL-28R Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient IFNLR1 upregulation across a broader range of human cell types.
IL-28R Lentiviral Activation Particles (h) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the IFNLR1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous IL-28R expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native IFNLR1 genomic locus and regulatory architecture.
The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.