
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FOXF2 CRISPR Activation Plasmid (h) | sc-404367-ACT | 20 µg | $397.00 |
FOXF2 (forkhead box F2) is a human forkhead family transcription factor that regulates mesenchymal differentiation, extracellular matrix remodeling, and epithelial–mesenchymal signaling during development and tissue homeostasis. It modulates transcriptional programs linked to cell motility, adhesion, and stromal–epithelial crosstalk, intersecting with pathways such as TGF-β–responsive gene regulation and broader developmental signaling networks. Altered FOXF2 expression has been associated with dysregulated differentiation states and changes in invasiveness-related gene expression programs in multiple disease contexts. These properties make FOXF2 a useful node for dissecting transcriptional control of lineage specification and microenvironment-driven phenotypes.
FOXF2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FOXF2 expression without altering the underlying DNA sequence.
FOXF2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FOXF2 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 FOXF2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FOXF2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FOXF2 locus and enabling the study of FOXF2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FOXF2 pathway restoration in tumor cells with silenced or reduced FOXF2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.