
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AIM2 CRISPR Activation Plasmid (h) | sc-403391-ACT | 20 µg | $397.00 |
Absent in melanoma 2 (AIM2) encodes a cytosolic pattern-recognition receptor that detects double-stranded DNA and assembles the AIM2 inflammasome, promoting ASC-dependent caspase-1 activation with downstream maturation of IL‑1β and IL‑18 and induction of pyroptotic cell death. AIM2 signaling intersects with innate immune sensing networks and inflammatory transcriptional programs, shaping antimicrobial responses and sterile inflammation. Dysregulated AIM2 activity has been implicated in inflammatory and autoimmune pathophysiology as well as tumor-associated inflammation, making it a useful node for studying DNA-triggered innate immunity and cytokine processing in human cells.
AIM2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous AIM2 expression without altering the underlying DNA sequence.
AIM2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the AIM2 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 AIM2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous AIM2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native AIM2 locus and enabling the study of AIM2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of AIM2 pathway restoration in tumor cells with silenced or reduced AIM2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.