
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Profilin-2 CRISPR Activation Plasmid (h) | sc-403456-ACT | 20 µg | $397.00 |
PFN2 encodes profilin-2, an actin monomer–binding protein that regulates actin polymerization dynamics and links cytoskeletal remodeling to membrane trafficking and signal transduction. Profilin-2 coordinates interactions with poly-L-proline–containing ligands and phosphoinositides, supporting processes such as neurite outgrowth, synaptic function, cell motility, and endocytosis. Through its role in actin cytoskeleton organization, PFN2 influences pathways governing adhesion, migration, and neuronal connectivity. Dysregulation of profilin-2–dependent actin remodeling has been investigated in the context of neurodevelopmental and neurodegenerative phenotypes as well as invasive cellular behavior.
Profilin-2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PFN2 expression without altering the underlying DNA sequence.
Profilin-2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PFN2 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 PFN2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Profilin-2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PFN2 locus and enabling the study of Profilin-2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Profilin-2 pathway restoration in tumor cells with silenced or reduced PFN2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.