Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
FKHRL1/FOXO3a CRISPR Activation Plasmid (h): sc-400308-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FKHRL1/FOXO3a CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- FKHRL1/FOXO3a CRISPR Activation Plasmid (h) 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 FKHRL1/FOXO3a CRISPR Activation Plasmid (h) and FKHRL1/FOXO3a CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the FOXO3 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: FKHRL1/FOXO3a Antibody (D-12): sc-48348
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FKHRL1/FOXO3a CRISPR Activation Plasmid (h) | sc-400308-ACT | 20 µg | $397.00 | |||
FKHRL1/FOXO3a CRISPR Activation Plasmid (h2) | sc-400308-ACT-2 | 20 µg | $397.00 |
FOXO3 (FKHRL1/FOXO3a) is a forkhead box transcription factor that integrates insulin/IGF-1–PI3K–AKT signaling with cellular stress responses to regulate genes controlling apoptosis, cell-cycle arrest, DNA damage repair, autophagy, and antioxidant defense. Phosphorylation by AKT promotes FOXO3 nuclear exclusion, while oxidative stress and AMPK-dependent cues favor nuclear activity and transcriptional programs linked to metabolic homeostasis and survival. FOXO3 also interfaces with TGF-β, MAPK, and mTOR pathways to shape differentiation and immune and inflammatory outputs across cell types. Altered FOXO3 regulation has been associated with tumor biology, neurodegenerative processes, cardiometabolic phenotypes, and aging-related traits, making it a common node for mechanistic studies of stress adaptation.
FKHRL1/FOXO3a CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FOXO3 expression without altering the underlying DNA sequence.
FKHRL1/FOXO3a CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FOXO3 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 FOXO3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FKHRL1/FOXO3a expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FOXO3 locus and enabling the study of FKHRL1/FOXO3a-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FKHRL1/FOXO3a pathway restoration in tumor cells with silenced or reduced FOXO3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.