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 Lentiviral Activation Particles (h): sc-400308-LAC
- Target species: human
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- FKHRL1/FOXO3a Lentiviral Activation Particles (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically and efficiently upregulate gene expression via lentiviral transduction of cells
- FKHRL1/FOXO3a Lentiviral Activation Particles (h) contain the following SAM Activation elements: a deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, an MS2-p65-HSF1 fusion protein and a target-specific 20 nt guide RNA. They also contain the blasticidin, hygromycin and puromycin resistance genes
- Upon transduction, the 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 Lentiviral Activation Plasmid (h) and FKHRL1/FOXO3a Lentiviral Activation Plasmid (h2) target distinct regulatory regions of the FOXO3 promoter. One or both designs may be available
- Following transfection, gene activation 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 Lentiviral Activation Particles (h) | sc-400308-LAC | 200 µl | $455.00 | |||
FKHRL1/FOXO3a Lentiviral Activation Particles (h2) | sc-400308-LAC-2 | 200 µl | $455.00 |
FOXO3 (FKHRL1/FOXO3a) is a forkhead box O transcription factor that coordinates cell fate decisions by regulating genes involved in apoptosis, cell-cycle arrest, DNA damage responses, oxidative stress resistance, and autophagy. Its activity is tightly controlled by post-translational modifications downstream of PI3K–AKT signaling, which modulate FOXO3 nuclear localization and transcriptional output, and it integrates inputs from AMPK and sirtuin pathways during metabolic stress. FOXO3-dependent programs influence immune homeostasis, stem/progenitor cell maintenance, and cellular senescence, linking this factor to aging-associated phenotypes. Dysregulated FOXO3 signaling has been implicated in tumor biology and resistance to stress, as well as cardiometabolic and neurodegenerative disease mechanisms through altered stress-response transcriptional networks.
FKHRL1/FOXO3a Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient FOXO3 upregulation across a broader range of human cell types.
FKHRL1/FOXO3a Lentiviral Activation Particles (h) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the FOXO3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous FKHRL1/FOXO3a expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native FOXO3 genomic locus and regulatory architecture.
The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.