PCTAIRE-3 Lentiviral Activation Particles (h): sc-404867-LAC

CDK18 encodes the serine/threonine kinase PCTAIRE-3, a cyclin-dependent kinase family member implicated in regulating cell-cycle progression and phosphorylation-dependent signaling in proliferating cells. CDK18 activity has been linked to genome maintenance and DNA damage response networks, including processes that influence replication stress and checkpoint control. Altered CDK18 expression or function has been associated with aberrant proliferation phenotypes and has been explored in the context of cancer biology and other disorders where cell-cycle and repair pathways are dysregulated. As a modulator of kinase-driven circuitry, CDK18 provides a useful node for interrogating pathway cross-talk between cyclin/CDK regulation, stress signaling, and transcriptional programs.

PCTAIRE-3 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 CDK18 upregulation across a broader range of human cell types.

PCTAIRE-3 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 CDK18 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous PCTAIRE-3 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native CDK18 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.