Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
IL-1 beta/IL1B CRISPR Activation Plasmid (h): sc-400078-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IL-1 beta/IL1B CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- IL-1 beta/IL1B 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-1 beta/IL1B CRISPR Activation Plasmid (h) and IL-1 beta/IL1B CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the IL1B 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-1 beta/IL1B Antibody (B122): sc-12742
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-1 beta/IL1B CRISPR Activation Plasmid (h) | sc-400078-ACT | 20 µg | $397.00 |
IL1B encodes interleukin-1 beta (IL-1β), a pro-inflammatory cytokine produced primarily by activated monocytes and macrophages and processed to its mature form following inflammasome-dependent caspase-1 cleavage. IL-1β signaling through IL1R1 and IL1RAP activates MyD88-dependent pathways that converge on NF-κB and MAPK cascades, driving transcriptional programs involved in leukocyte recruitment, fever, and acute-phase responses. This axis shapes innate immune activation, pyroptosis-associated inflammatory outputs, and crosstalk with cytokines such as IL-6 and TNF. Dysregulated IL1B expression and inflammasome activity are implicated in chronic inflammatory and autoimmune pathologies, metabolic inflammation, and tumor-associated inflammation in multiple tissue contexts.
IL-1 beta/IL1B CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous IL1B expression without altering the underlying DNA sequence.
IL-1 beta/IL1B CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the IL1B 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 IL1B transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IL-1 beta/IL1B expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native IL1B locus and enabling the study of IL-1 beta/IL1B-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IL-1 beta/IL1B pathway restoration in tumor cells with silenced or reduced IL1B expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.