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.
Cryopyrin/NALP3/NLRP3 CRISPR Activation Plasmid (h): sc-400270-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Cryopyrin/NALP3/NLRP3 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Cryopyrin/NALP3/NLRP3 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 Cryopyrin/NALP3/NLRP3 CRISPR Activation Plasmid (h) and Cryopyrin/NALP3/NLRP3 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the NLRP3 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: Cryopyrin/NALP3/NLRP3 Antibody (6F12): sc-134306
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Cryopyrin/NALP3/NLRP3 CRISPR Activation Plasmid (h) | sc-400270-ACT | 20 µg | $397.00 |
NLRP3 (cryopyrin/NALP3) is a cytosolic pattern-recognition receptor that nucleates the NLRP3 inflammasome in response to diverse cellular stress signals, including ionic flux, mitochondrial dysfunction, lysosomal damage, and reactive oxygen species. Inflammasome assembly promotes ASC recruitment and caspase-1 activation, driving processing and secretion of IL-1β and IL-18 and enabling gasdermin D–dependent pyroptosis. This axis integrates innate immune signaling with metabolic and danger-sensing pathways, shaping leukocyte activation, tissue inflammation, and host defense. Dysregulated NLRP3 activity is implicated in autoinflammatory and inflammatory disease mechanisms, making it a key target for studying inflammasome regulation, cytokine maturation, and cell death programs in human systems.
Cryopyrin/NALP3/NLRP3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous NLRP3 expression without altering the underlying DNA sequence.
Cryopyrin/NALP3/NLRP3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the NLRP3 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 NLRP3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Cryopyrin/NALP3/NLRP3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native NLRP3 locus and enabling the study of Cryopyrin/NALP3/NLRP3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Cryopyrin/NALP3/NLRP3 pathway restoration in tumor cells with silenced or reduced NLRP3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.