FGF-BP CRISPR Activation Plasmid (h): sc-404956-ACT

FGFBP1 encodes fibroblast growth factor–binding protein 1 (FGF-BP), a secreted carrier that mobilizes heparin-bound FGFs from the extracellular matrix and enhances FGF signaling bioavailability. By potentiating ligand–receptor interactions, FGF-BP can influence MAPK/ERK- and PI3K/AKT-linked processes including cell proliferation, migration, and angiogenic remodeling in tissue microenvironments. Altered FGFBP1 expression has been reported across multiple disease contexts and is frequently studied as a modulator of growth factor–driven phenotypes, extracellular matrix dynamics, and stromal–epithelial communication. These properties make FGFBP1 a useful node for mechanistic studies of FGF pathway regulation and secreted proteome contributions to cellular state changes.

FGF-BP CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FGFBP1 expression without altering the underlying DNA sequence.

FGF-BP CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FGFBP1 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 FGFBP1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FGF-BP expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FGFBP1 locus and enabling the study of FGF-BP-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FGF-BP pathway restoration in tumor cells with silenced or reduced FGFBP1 expression.

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