FGF-18 CRISPR Activation Plasmid (h): sc-402175-ACT

FGF18 encodes fibroblast growth factor 18 (FGF-18), a secreted mitogen that signals primarily through FGFR family receptor tyrosine kinases to regulate cell proliferation, survival, and lineage specification. In human tissues, FGF-18 contributes to developmental and homeostatic programs, including chondrogenesis and osteogenesis, by engaging MAPK/ERK and PI3K/AKT pathway activity and shaping extracellular matrix remodeling. Altered FGF/FGFR signaling dynamics are frequently studied in contexts of aberrant growth control, tissue remodeling, and tumor-associated microenvironmental crosstalk. As a pathway node with broad effects on differentiation and mitogenic signaling, FGF18 is commonly interrogated in models of skeletal biology, stromal signaling, and growth factor–dependent transcriptional programs.

FGF-18 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FGF18 expression without altering the underlying DNA sequence.

FGF-18 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FGF18 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 FGF18 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FGF-18 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FGF18 locus and enabling the study of FGF-18-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FGF-18 pathway restoration in tumor cells with silenced or reduced FGF18 expression.

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