FGF-13 CRISPR Activation Plasmid (m): sc-420327-ACT

Mouse Fgf13 encodes fibroblast growth factor 13 (FGF-13), an intracellular member of the FGF family that functions predominantly outside of canonical secreted FGF/FGFR signaling. FGF-13 associates with microtubules and modulates cytoskeletal dynamics, neurite outgrowth, and neuronal polarization, and it has been linked to regulation of voltage-gated sodium channel activity that shapes excitability in the nervous system. Through these roles, FGF-13 intersects with pathways governing axonal development, synaptic function, and activity-dependent neuronal maturation. Dysregulated FGF-13 expression or function has been implicated in neurodevelopmental and neuropsychiatric phenotypes, supporting its use in studies of circuit formation and excitability-related disease mechanisms.

FGF-13 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Fgf13 expression without altering the underlying DNA sequence.

FGF-13 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Fgf13 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 Fgf13 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FGF-13 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Fgf13 locus and enabling the study of FGF-13-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FGF-13 pathway restoration in tumor cells with silenced or reduced Fgf13 expression.

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