IL-1RAcP CRISPR Activation Plasmid (h): sc-402026-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IL-1RAcP CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- IL-1RAcP 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-1RAcP CRISPR Activation Plasmid (h) and IL-1RAcP CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the IL1RAP transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: IL-1RAcP Antibody (D-5): sc-376872
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-1RAcP CRISPR Activation Plasmid (h) | sc-402026-ACT | 20 µg | $397.00 |
IL1RAP encodes interleukin-1 receptor accessory protein (IL-1RAcP), an essential co-receptor that heterodimerizes with IL1R1 or IL1RL1 (ST2) to propagate signaling triggered by IL-1 family cytokines. Upon ligand engagement, IL-1RAcP helps assemble the receptor complex and recruit adaptor proteins such as MyD88, initiating IRAK-dependent cascades that activate NF-κB and MAPK pathways to regulate inflammatory gene expression. This signaling axis influences innate immune activation, cytokine production, and cross-talk with inflammasome-driven responses. Dysregulated IL1RAP-associated signaling is frequently studied in the context of chronic inflammation and tumor microenvironment–associated immune modulation, making it relevant for mechanistic studies in immunology and oncology models.
IL-1RAcP CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous IL1RAP expression without altering the underlying DNA sequence.
IL-1RAcP CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the IL1RAP 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 IL1RAP transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IL-1RAcP expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native IL1RAP locus and enabling the study of IL-1RAcP-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IL-1RAcP pathway restoration in tumor cells with silenced or reduced IL1RAP expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.