ISGF-3γ p48 CRISPR Activation Plasmid (m): sc-421156-ACT
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ISGF-3γ p48 CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- ISGF-3γ p48 CRISPR Activation Plasmid (m) 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 ISGF-3γ p48 CRISPR Activation Plasmid (m) and ISGF-3γ p48 CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Irf9 transcriptional start site. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ISGF-3γ p48 CRISPR Activation Plasmid (m) | sc-421156-ACT | 20 µg | $397.00 |
Interferon regulatory factor 9 (Irf9), also known as ISGF-3γ p48, encodes a DNA-binding component of the interferon-stimulated gene factor 3 (ISGF3) complex that cooperates with STAT1 and STAT2 to transduce type I and type III interferon signals. Following interferon receptor engagement and JAK/STAT activation, IRF9 helps direct ISGF3 to interferon-stimulated response elements (ISREs), coordinating transcriptional programs involved in antiviral defense, antigen presentation, and innate immune regulation. In mouse models, Irf9 activity influences cytokine signaling networks and crosstalk between interferon pathways and broader inflammatory programs. Dysregulated IRF9-dependent transcription has been investigated in contexts of altered immune responsiveness, chronic inflammation, and host–pathogen interactions relevant to immune-mediated disease mechanisms.
ISGF-3γ p48 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Irf9 expression without altering the underlying DNA sequence.
ISGF-3γ p48 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Irf9 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 Irf9 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ISGF-3γ p48 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Irf9 locus and enabling the study of ISGF-3γ p48-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ISGF-3γ p48 pathway restoration in tumor cells with silenced or reduced Irf9 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.