periaxin CRISPR Activation Plasmid (h): sc-404868-ACT

PRX encodes periaxin, a Schwann cell–enriched protein that scaffolds the abaxonal cytoplasm and supports myelin sheath stability in the peripheral nervous system. Periaxin participates in cytoskeletal organization and membrane-associated complexes that help maintain internodal architecture, including interactions with dystroglycan- and laminin-associated structures. Through these structural roles, PRX contributes to axon–glia communication, myelin maintenance, and peripheral nerve conduction. Disruption of PRX function is linked to inherited peripheral neuropathies characterized by demyelination and impaired nerve physiology, making it a relevant target for mechanistic studies of myelin biology.

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

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

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