Cdc6 Lentiviral Activation Particles (h): sc-400796-LAC

Human CDC6 encodes Cdc6, a core AAA+ ATPase required for DNA replication origin licensing and pre-replication complex assembly, coordinating with ORC and MCM loading during late mitosis and G1. Cdc6 activity is tightly regulated by CDK-dependent phosphorylation and ubiquitin-mediated turnover to prevent re-replication and maintain genome stability. Dysregulated CDC6 expression has been linked to replication stress, checkpoint activation, and chromosomal instability, processes frequently studied in oncogenesis and proliferative disorders. As a replication-licensing factor, Cdc6 is routinely used to interrogate cell-cycle control, S-phase entry, and DNA damage response signaling in human model systems.

Cdc6 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 CDC6 upregulation across a broader range of human cell types.

Cdc6 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 CDC6 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Cdc6 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native CDC6 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.