ARK-2 Lentiviral Activation Particles (h): sc-402041-LAC

AURKB encodes aurora kinase B (ARK-2), a serine/threonine kinase that functions as the catalytic core of the chromosomal passenger complex to coordinate chromosome condensation, kinetochore–microtubule attachments, spindle checkpoint signaling, and cytokinesis. By phosphorylating substrates such as histone H3 and key centromere/kinetochore proteins, AURKB regulates error correction during mitosis and ensures faithful chromosome segregation. Dysregulated AURKB activity is linked to chromosomal instability, aneuploidy, and altered proliferative control observed in multiple tumor contexts, making it a widely used node for studying mitotic control and genome maintenance. Experimental modulation of AURKB supports investigations into cell-cycle transitions, spindle assembly checkpoint dynamics, and mechanisms of replication stress tolerance.

ARK-2 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 AURKB upregulation across a broader range of human cell types.

ARK-2 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 AURKB transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous ARK-2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native AURKB 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.