TBX2 Lentiviral Activation Particles (h): sc-403078-LAC

TBX2 encodes a T-box transcription factor that binds sequence-specific DNA elements to regulate developmental gene expression programs and cell-cycle progression. In human cells, TBX2 often functions as a transcriptional repressor that helps control proliferation, senescence bypass, and lineage specification through coordination with chromatin remodeling and corepressor complexes. Its activity intersects with pathways governing G1/S control and differentiation, and dysregulated TBX2 expression has been reported in multiple tumor contexts where it can influence growth and invasive phenotypes. As a nuclear regulator, TBX2 is frequently studied for its role in transcriptional networks that shape organogenesis, epithelial–mesenchymal dynamics, and stress-response programs.

TBX2 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 TBX2 upregulation across a broader range of human cell types.

TBX2 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 TBX2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TBX2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native TBX2 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.