
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
G1P3 CRISPR Activation Plasmid (h) | sc-403682-ACT | 20 µg | $397.00 |
Human IFI6 (G1P3) encodes an interferon-stimulated, membrane-associated protein that modulates innate immune signaling and cellular stress responses. IFI6 is induced downstream of type I interferon/JAK–STAT signaling and has been linked to regulation of mitochondrial integrity, apoptosis sensitivity, and antiviral restriction programs that reshape transcriptional networks. Altered IFI6 expression has been reported across inflammatory contexts and multiple cancers, where it correlates with interferon pathway activation and changes in cell survival and proliferation. As a result, IFI6 serves as a useful node for interrogating interferon-driven pathways, host–pathogen interactions, and stress-adaptation phenotypes in human cells.
G1P3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous IFI6 expression without altering the underlying DNA sequence.
G1P3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the IFI6 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 IFI6 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous G1P3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native IFI6 locus and enabling the study of G1P3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of G1P3 pathway restoration in tumor cells with silenced or reduced IFI6 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.