PTPζ CRISPR Activation Plasmid (h): sc-401775-ACT

PTPRZ1 encodes protein tyrosine phosphatase receptor type Z1 (PTPζ), a receptor-like phosphatase enriched in the central nervous system that modulates tyrosine phosphorylation states at the cell surface. PTPζ integrates extracellular cues from ligands such as pleiotrophin and midkine to influence cell adhesion, migration, and neurite outgrowth, interfacing with signaling networks that include SRC family kinases, MAPK/ERK, and PI3K/AKT pathways. Through regulation of glial and neural progenitor behaviors, PTPRZ1 contributes to developmental and activity-dependent processes in neural tissue. Altered PTPRZ1 expression or signaling has been associated with neuroinflammatory states, demyelinating pathology, and glioma biology, supporting its use in mechanistic studies of neural signaling and microenvironmental interactions.

PTPζ CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PTPRZ1 expression without altering the underlying DNA sequence.

PTPζ CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PTPRZ1 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 PTPRZ1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PTPζ expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PTPRZ1 locus and enabling the study of PTPζ-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PTPζ pathway restoration in tumor cells with silenced or reduced PTPRZ1 expression.

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