TPX2 Lentiviral Activation Particles (h): sc-402581-LAC

TPX2 (targeting protein for Xklp2) encodes a microtubule-associated spindle assembly factor that concentrates at centrosomes and spindle microtubules to promote Aurora A kinase activation and stabilize kinetochore fibers during mitosis. By coordinating microtubule nucleation, spindle pole organization, and chromosome segregation, TPX2 helps govern cell-cycle progression through the G2/M transition and supports fidelity of mitotic checkpoint control. Dysregulated TPX2 expression is frequently associated with proliferative phenotypes and genomic instability, making it a widely used marker and mechanistic node in studies of aneuploidy, mitotic stress responses, and tumor biology. TPX2-dependent signaling intersects with pathways controlling microtubule dynamics, centrosome function, and Aurora kinase–regulated phosphorylation networks.

TPX2 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 TPX2 upregulation across a broader range of human cell types.

TPX2 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 TPX2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TPX2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native TPX2 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.