FGF-10 CRISPR Activation Plasmid (h): sc-417825-ACT

FGF10 encodes fibroblast growth factor 10 (FGF-10), a secreted paracrine ligand that primarily signals through FGFR2b to regulate epithelial–mesenchymal crosstalk during organogenesis and adult tissue homeostasis. FGF-10 activates canonical receptor tyrosine kinase pathways including RAS–MAPK/ERK, PI3K–AKT, and PLCγ signaling to control proliferation, migration, survival, and branching morphogenesis. Dysregulated FGF10–FGFR2b signaling has been implicated in abnormal lung and gland development, impaired wound repair, and altered epithelial growth programs relevant to congenital disorders and cancer biology. As a developmental morphogen and niche factor, FGF-10 is commonly studied in airway epithelium, mammary and salivary gland biology, and stromal–epithelial signaling models.

FGF-10 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FGF10 expression without altering the underlying DNA sequence.

FGF-10 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FGF10 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 FGF10 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FGF-10 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FGF10 locus and enabling the study of FGF-10-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FGF-10 pathway restoration in tumor cells with silenced or reduced FGF10 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.