
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Profilin-1 CRISPR Activation Plasmid (h) | sc-402070-ACT | 20 µg | $397.00 |
PFN1 encodes profilin-1, a conserved actin-binding protein that regulates actin monomer availability and promotes controlled actin polymerization, shaping cytoskeletal dynamics, membrane ruffling, and cell motility. Profilin-1 interfaces with proline-rich ligands and phosphoinositide signaling, linking actin remodeling to pathways governing endocytosis, adhesion, and mechanotransduction. Through its central role in cytoskeletal organization, PFN1 is frequently studied in contexts of neuronal integrity, migration, and stress responses. Altered PFN1 expression or function has been associated with dysregulated actin dynamics observed in neurodegenerative and cancer-related cellular phenotypes, making it a useful target for pathway-focused investigation.
Profilin-1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PFN1 expression without altering the underlying DNA sequence.
Profilin-1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PFN1 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 PFN1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Profilin-1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PFN1 locus and enabling the study of Profilin-1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Profilin-1 pathway restoration in tumor cells with silenced or reduced PFN1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.