FOXE3 CRISPR Activation Plasmid (h): sc-404466-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FOXE3 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- FOXE3 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 FOXE3 CRISPR Activation Plasmid (h) and FOXE3 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the FOXE3 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: FOXE3 Antibody (G-1): sc-393526
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FOXE3 CRISPR Activation Plasmid (h) | sc-404466-ACT | 20 µg | $397.00 |
FOXE3 (forkhead box E3) encodes a forkhead/winged-helix transcription factor that regulates gene expression programs required for ocular development, particularly lens placode formation, lens epithelial maintenance, and differentiation. Through sequence-specific DNA binding, FOXE3 coordinates transcriptional networks that influence cell-cycle control, epithelial identity, and lineage commitment in anterior segment tissues. Dysregulated FOXE3 function and genetic variants are linked to congenital eye disorders, including anterior segment dysgenesis, microphthalmia, and cataract-associated phenotypes, making it a relevant target for studying developmental transcriptional control. FOXE3 is therefore widely used as a molecular handle to model lens biology and to map upstream regulators and downstream effectors of forkhead-factor signaling.
FOXE3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FOXE3 expression without altering the underlying DNA sequence.
FOXE3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FOXE3 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 FOXE3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FOXE3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FOXE3 locus and enabling the study of FOXE3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FOXE3 pathway restoration in tumor cells with silenced or reduced FOXE3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.