PTPκ Lentiviral Activation Particles (h): sc-402287-LAC

Human PTPRK encodes protein tyrosine phosphatase receptor type K (PTPκ), a transmembrane phosphatase that modulates tyrosine phosphorylation at the cell surface and helps coordinate signals governing cell–cell adhesion, junctional integrity, and cytoskeletal organization. Through regulation of receptor and non-receptor kinase signaling, PTPκ influences pathways linked to contact inhibition, epithelial barrier function, and migratory behavior. Altered PTPRK activity or expression has been associated with dysregulated phosphorylation networks in cancer-related processes, including invasion and changes in tissue architecture. These features make PTPRK a useful node for studying how phosphatase-mediated dephosphorylation shapes signaling dynamics in human cells.

PTPκ Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient PTPRK upregulation across a broader range of human cell types.

PTPκ Lentiviral Activation Particles (h) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the PTPRK transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous PTPκ expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native PTPRK genomic locus and regulatory architecture.

The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.

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