PTP-MEG2 CRISPR Activation Plasmid (h): sc-402658-ACT

PTPN9 encodes the protein tyrosine phosphatase PTP-MEG2, a cytosolic regulator of phosphotyrosine signaling that counterbalances kinase-driven pathways controlling vesicle trafficking, secretion, and receptor-proximal signal transduction. PTP-MEG2 has been implicated in the modulation of immune-cell signaling outputs and growth-factor–responsive processes by dephosphorylating key substrates at membranes and secretory compartments. Through these activities, PTPN9 influences cellular homeostasis programs including adhesion, migration, and metabolic signaling. Altered PTPN9 expression or signaling context has been associated in the literature with dysregulated inflammatory signaling and oncogenic network rewiring, supporting its utility as a mechanistic node in pathway-focused studies.

PTP-MEG2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PTPN9 expression without altering the underlying DNA sequence.

PTP-MEG2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PTPN9 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 PTPN9 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PTP-MEG2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PTPN9 locus and enabling the study of PTP-MEG2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PTP-MEG2 pathway restoration in tumor cells with silenced or reduced PTPN9 expression.

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