PKC beta Lentiviral Activation Particles (h): sc-400263-LAC

PRKCB encodes protein kinase C beta (PKCβ), a diacylglycerol- and Ca²⁺-responsive serine/threonine kinase that links receptor-driven phospholipase C signaling to phosphorylation programs controlling proliferation, differentiation, migration, and survival. PKCβ functions downstream of antigen receptors and Fc receptors to shape B-cell activation and innate immune signaling, and it modulates endothelial and platelet responses through regulation of cytoskeletal dynamics and secretion. In cancer biology, PRKCB-dependent signaling intersects with MAPK/ERK, NF-κB, and PI3K pathway outputs that influence cell-state transitions and stress responses, while dysregulation has also been associated with inflammatory and vascular pathophysiology. These features make PRKCB a useful node for probing signal transduction mechanisms, phosphorylation-dependent pathway crosstalk, and context-specific transcriptional programs in human cell models.

PKC beta 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 PRKCB upregulation across a broader range of human cell types.

PKC beta 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 PRKCB transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous PKC beta expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native PRKCB 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.