IFN-γ/Interferon gamma CRISPR Activation Plasmid (m): sc-421050-ACT
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IFN-γ/Interferon gamma CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- IFN-γ/Interferon gamma 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 IFN-γ/Interferon gamma CRISPR Activation Plasmid (m) and IFN-γ/Interferon gamma CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Ifng 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: IFN-γ/Interferon gamma Antibody (G-30): sc-57208
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IFN-γ/Interferon gamma CRISPR Activation Plasmid (m) | sc-421050-ACT | 20 µg | $397.00 | |||
IFN-γ/Interferon gamma CRISPR Activation Plasmid (m2) | sc-421050-ACT-2 | 20 µg | $397.00 |
Mouse Ifng encodes interferon gamma (IFN-γ), a pleiotropic type II interferon that coordinates innate and adaptive immune responses by activating macrophages and shaping T helper 1 polarization. IFN-γ signals primarily through IFNGR1/IFNGR2 to engage JAK1/JAK2 and STAT1, inducing interferon-stimulated genes that enhance antigen processing and presentation, antimicrobial defenses, and immunoregulatory feedback. This cytokine intersects with NF-κB- and IRF-driven transcriptional programs, influencing chemokine production, MHC expression, and cellular differentiation states. Dysregulated IFN-γ activity is implicated in inflammatory and autoimmune pathology, host-pathogen susceptibility, tumor immune surveillance, and neuroinflammatory processes, making Ifng a central node for mechanistic immunology studies.
IFN-γ/Interferon gamma CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Ifng expression without altering the underlying DNA sequence.
IFN-γ/Interferon gamma CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Ifng 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 Ifng transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IFN-γ/Interferon gamma expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Ifng locus and enabling the study of IFN-γ/Interferon gamma-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IFN-γ/Interferon gamma pathway restoration in tumor cells with silenced or reduced Ifng expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.