
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-13Rα2 CRISPR Activation Plasmid (h) | sc-402525-ACT | 20 µg | $397.00 | |||
IL-13Rα2 CRISPR Activation Plasmid (h2) | sc-402525-ACT-2 | 20 µg | $397.00 |
Human IL13RA2 encodes interleukin-13 receptor alpha 2 (IL-13Rα2), a high-affinity IL-13 binding subunit that modulates type 2 cytokine signaling at the cell surface. By shaping IL-13-driven responses and receptor complex dynamics, IL-13Rα2 influences downstream programs linked to inflammatory signaling and cellular state transitions, including pathways that intersect with JAK/STAT- and MAPK-associated transcriptional outputs depending on cellular context. IL13RA2 expression is frequently used as a marker of altered cytokine responsiveness and has been associated with tumor biology, immune microenvironment interactions, and neuroinflammatory processes. These properties make IL-13Rα2 a useful target for mechanistic studies of cytokine receptor regulation, ligand sequestration, and signaling rewiring in disease-relevant models.
IL-13Rα2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous IL13RA2 expression without altering the underlying DNA sequence.
IL-13Rα2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the IL13RA2 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 IL13RA2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IL-13Rα2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native IL13RA2 locus and enabling the study of IL-13Rα2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IL-13Rα2 pathway restoration in tumor cells with silenced or reduced IL13RA2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.