TBX5 Lentiviral Activation Particles (m): sc-423282-LAC

Mouse Tbx5 encodes TBX5, a T-box transcription factor that binds sequence-specific DNA motifs to coordinate gene regulatory programs during embryonic development and tissue patterning. TBX5 is a core determinant of cardiac morphogenesis and forelimb specification, integrating transcriptional networks that control cardiomyocyte differentiation, chamber formation, and conduction system maturation. It functions in concert with other lineage factors such as NKX2-5 and GATA proteins to regulate enhancers controlling structural and electrophysiological genes. Dysregulated TBX5 dosage or activity is linked to congenital heart and limb malformations, making it a valuable node for studying developmental gene regulation and genotype–phenotype relationships in mouse models.

TBX5 Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Tbx5 upregulation across a broader range of human cell types.

TBX5 Lentiviral Activation Particles (m) 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 Tbx5 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TBX5 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Tbx5 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.