
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-17RB CRISPR Activation Plasmid (h) | sc-404114-ACT | 20 µg | $397.00 |
IL17RB encodes interleukin-17 receptor B (IL-17RB), a type I transmembrane cytokine receptor that partners with IL17RA to transduce signals from IL-17 family ligands, most prominently IL-25 (IL-17E). Receptor engagement recruits adaptor proteins such as ACT1 to stimulate NF-κB and MAPK signaling programs, linking epithelial and stromal sensing to chemokine production, mucosal inflammation, and type 2 immune polarization. IL-17RB activity influences crosstalk among airway and barrier tissues, myeloid cells, and lymphoid subsets, shaping responses to allergens and helminths as well as broader inflammatory remodeling. Dysregulated IL17RB expression or signaling has been associated with chronic inflammatory states and tumor-associated immune microenvironment changes, making it relevant for mechanistic studies of immune signaling and cell–cell communication.
IL-17RB CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous IL17RB expression without altering the underlying DNA sequence.
IL-17RB CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the IL17RB 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 IL17RB transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IL-17RB expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native IL17RB locus and enabling the study of IL-17RB-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IL-17RB pathway restoration in tumor cells with silenced or reduced IL17RB expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.