PTPσ CRISPR Activation Plasmid (h): sc-402631-ACT

PTPRS encodes protein tyrosine phosphatase receptor type S (PTPσ), a receptor-type phosphatase that modulates phosphorylation-dependent signaling at the cell surface. PTPσ participates in cell adhesion, axon guidance, and synapse organization by integrating extracellular matrix and proteoglycan cues with intracellular kinase pathways controlling cytoskeletal dynamics and neurite outgrowth. In the nervous system, altered PTPσ signaling has been associated with impaired regenerative responses and synaptic remodeling, while in oncology contexts PTPRS dysregulation has been linked to perturbed growth factor signaling and changes in cell migration. These biology features make PTPRS a useful target for dissecting phosphotyrosine signaling networks governing differentiation, connectivity, and invasive phenotypes in human cell models.

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

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

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