
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRα Lentiviral Activation Particles (h) | sc-401475-LAC | 200 µl | $455.00 |
THRA encodes thyroid hormone receptor alpha (TRα), a ligand-activated nuclear receptor that binds triiodothyronine (T3) and regulates transcription through thyroid hormone response elements. TRα coordinates developmental and metabolic gene programs by modulating chromatin accessibility and coregulator recruitment, influencing processes such as cell differentiation, mitochondrial bioenergetics, and cell-cycle control. As a central node in thyroid hormone signaling, THRA contributes to tissue-specific endocrine responsiveness and cross-talk with MAPK/PI3K and retinoid receptor pathways. Dysregulated TRα signaling or altered receptor function is relevant to endocrine and metabolic phenotypes and can impact lineage specification programs studied in neurodevelopmental and cardiometabolic research models.
TRα 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 THRA upregulation across a broader range of human cell types.
TRα 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 THRA transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TRα expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native THRA 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.