
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TEF-1 Lentiviral Activation Particles (h) | sc-402607-LAC | 200 µl | $455.00 |
TEAD1 encodes TEF-1, a TEA/ATTS domain transcription factor that partners with YAP/TAZ to regulate gene programs controlling cell proliferation, survival, differentiation, and tissue growth. TEF-1 is a key nuclear effector of Hippo signaling and integrates inputs from mechanotransduction, GPCR signaling, and cytoskeletal dynamics to modulate enhancer and promoter activity. Dysregulated TEAD1/TEF-1–dependent transcription has been linked to altered organ development and regeneration, and is frequently studied in the context of YAP/TAZ-driven transcriptional rewiring in cancer biology. TEAD1 activity is also relevant to cardiovascular and skeletal muscle gene expression programs, making it a useful node for investigating lineage specification and stress-responsive transcription.
TEF-1 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 TEAD1 upregulation across a broader range of human cell types.
TEF-1 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 TEAD1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TEF-1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native TEAD1 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.