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.
caspase-5 p10 CRISPR Activation Plasmid (h): sc-401520-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- caspase-5 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- caspase-5 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 caspase-5 CRISPR Activation Plasmid (h) and caspase-5 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the CASP5 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: caspase-5 p20 Antibody (H-2): sc-393346
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
caspase-5 p10 CRISPR Activation Plasmid (h) | sc-401520-ACT | 20 µg | $397.00 |
Human CASP5 encodes caspase-5, an inflammatory caspase whose p10 small subunit is generated during proteolytic maturation of the zymogen and contributes to formation of the active protease complex. CASP5 participates in innate immune signaling downstream of cytosolic danger sensing, promoting inflammatory caspase activity that can drive pyroptotic cell death and cytokine processing, often in coordination with inflammasome pathways. Its expression and activation state are studied in contexts of infection, sterile inflammation, and myeloid cell activation, where dysregulated inflammatory caspase signaling can influence tissue injury phenotypes. CASP5 is therefore relevant to mechanisms linking pattern-recognition signaling, cell death programs, and inflammatory gene expression networks.
caspase-5 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CASP5 expression without altering the underlying DNA sequence.
caspase-5 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CASP5 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 CASP5 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous caspase-5 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CASP5 locus and enabling the study of caspase-5-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of caspase-5 pathway restoration in tumor cells with silenced or reduced CASP5 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.