IL-11Rα CRISPR Activation Plasmid (h): sc-402503-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IL-11Rα CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- IL-11Rα 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-11Rα CRISPR Activation Plasmid (h) and IL-11Rα CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the IL11RA 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-11Rα Antibody (4D12): sc-130920
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-11Rα CRISPR Activation Plasmid (h) | sc-402503-ACT | 20 µg | $397.00 | |||
IL-11Rα CRISPR Activation Plasmid (h2) | sc-402503-ACT-2 | 20 µg | $397.00 |
IL11RA encodes the human interleukin-11 receptor alpha (IL-11Rα), the ligand-binding subunit that partners with the gp130 co-receptor to initiate signaling in response to IL-11. Receptor engagement activates JAK/STAT signaling, with additional contributions from MAPK/ERK and PI3K/AKT pathways, shaping transcriptional programs that regulate cell survival, proliferation, and differentiation in multiple stromal and epithelial contexts. IL-11Rα-dependent signaling is frequently studied in fibro-inflammatory processes, extracellular matrix remodeling, and tissue homeostasis, and altered pathway activity has been associated with fibrosis- and inflammation-linked disease biology. As a surface receptor with defined upstream ligand control and downstream transcriptional outputs, IL11RA is a useful node for dissecting cytokine signaling dynamics and pathway cross-talk in human cell models.
IL-11Rα CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous IL11RA expression without altering the underlying DNA sequence.
IL-11Rα CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the IL11RA 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 IL11RA transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IL-11Rα expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native IL11RA locus and enabling the study of IL-11Rα-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IL-11Rα pathway restoration in tumor cells with silenced or reduced IL11RA expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.