IL-17RA CRISPR Activation Plasmid (h): sc-401447-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IL-17RA CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- IL-17RA CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by IL-17RA CRISPR Activation Plasmid (h) and IL-17RA CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the IL17RA transcriptional start site. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-17RA CRISPR Activation Plasmid (h) | sc-401447-ACT | 20 µg | $397.00 | |||
IL-17RA CRISPR Activation Plasmid (h2) | sc-401447-ACT-2 | 20 µg | $397.00 |
IL17RA encodes interleukin-17 receptor A (IL-17RA), a widely expressed receptor subunit that pairs with IL-17RC to mediate signaling by IL-17A and IL-17F and can also participate in receptor complexes for other IL-17 family cytokines. Ligand engagement activates ACT1/TRAF6-dependent cascades that converge on NF-κB, MAPK, and C/EBP pathways, promoting transcription of chemokines, cytokines, and antimicrobial effectors that coordinate neutrophil recruitment and epithelial barrier immunity. IL-17RA signaling shapes inflammatory programs at mucosal and stromal surfaces and intersects with innate and adaptive immune responses, including Th17-driven biology. Dysregulated IL-17RA pathway activity has been linked to chronic inflammatory and autoimmune disease mechanisms and can influence tumor-associated inflammation and tissue remodeling in diverse contexts.
IL-17RA CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous IL17RA expression without altering the underlying DNA sequence.
IL-17RA CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the IL17RA 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 IL17RA transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IL-17RA expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native IL17RA locus and enabling the study of IL-17RA-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IL-17RA pathway restoration in tumor cells with silenced or reduced IL17RA expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.