STK33 Lentiviral Activation Particles (h): sc-404127-LAC

STK33 encodes a serine/threonine protein kinase implicated in the regulation of intracellular signaling networks that coordinate cell cycle progression, cytoskeletal dynamics, and cellular stress responses. As a kinase, STK33 can modulate phosphorylation-dependent pathways that influence transcriptional programs and protein stability, linking upstream cues to downstream changes in proliferation and survival. Altered STK33 expression or activity has been investigated in the context of oncogenic signaling dependencies and aberrant growth control in multiple tumor models. These features make STK33 a useful target for mechanistic studies of kinase-regulated signaling, pathway crosstalk, and genotype-dependent vulnerabilities in human cells.

STK33 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 STK33 upregulation across a broader range of human cell types.

STK33 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 STK33 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous STK33 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native STK33 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.