
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IFI-44 CRISPR Activation Plasmid (h) | sc-405329-ACT | 20 µg | $397.00 |
Human IFI44 (interferon-induced protein 44; IFI-44) is an interferon-stimulated gene induced downstream of type I and type III interferon signaling, integrating inputs from pattern-recognition receptor pathways such as RIG-I-like receptors and cGAS–STING. IFI-44 expression is commonly used as a readout of JAK–STAT-driven antiviral transcriptional programs and broader innate immune activation. Dysregulated IFI44 levels have been reported across inflammatory and autoimmune contexts and in infection-associated transcriptional signatures, linking it to disease-relevant interferon biology. In research settings, IFI44 serves as a molecular handle to interrogate interferon response amplitude, innate immune network connectivity, and stress-responsive gene regulation.
IFI-44 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous IFI44 expression without altering the underlying DNA sequence.
IFI-44 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the IFI44 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 IFI44 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IFI-44 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native IFI44 locus and enabling the study of IFI-44-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IFI-44 pathway restoration in tumor cells with silenced or reduced IFI44 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.