TrxR2 Lentiviral Activation Particles (h): sc-402671-LAC

TXNRD2 encodes the mitochondrial thioredoxin reductase TrxR2, a selenoprotein that maintains thioredoxin-2 in its reduced state to support mitochondrial redox homeostasis. By supplying reducing equivalents to the thioredoxin system, TrxR2 helps control reactive oxygen species, protein disulfide balance, and redox-sensitive signaling that influences apoptosis and cellular stress responses. TXNRD2 activity intersects with mitochondrial antioxidant networks and oxidative phosphorylation, linking it to processes such as metabolic adaptation and maintenance of mitochondrial integrity. Altered TXNRD2/TrxR2 function has been associated with oxidative stress–related phenotypes and is studied in contexts including neurodegeneration, cardiometabolic dysfunction, and cancer biology where mitochondrial redox control is a key variable.

TrxR2 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 TXNRD2 upregulation across a broader range of human cell types.

TrxR2 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 TXNRD2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TrxR2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native TXNRD2 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.