TPPP Lentiviral Activation Particles (h): sc-405957-LAC

Human TPPP (tubulin polymerization promoting protein) is a microtubule-associated factor enriched in oligodendrocytes that promotes tubulin assembly and stabilizes microtubule networks required for process extension and cellular morphology. By modulating cytoskeletal dynamics, TPPP influences myelin-related differentiation programs and intracellular transport processes that depend on microtubule organization. Altered TPPP expression or mislocalization has been linked to neurodegenerative pathology, where cytoskeletal disruption and aberrant protein aggregation are prominent cellular features. These properties make TPPP a useful node for studying microtubule regulation, oligodendrocyte biology, and pathways underlying neuronal-glial dysfunction.

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

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