TUSC3 Lentiviral Activation Particles (h): sc-405571-LAC

TUSC3 (tumor suppressor candidate 3) encodes an endoplasmic reticulum–localized subunit of the oligosaccharyltransferase (OST) complex that supports N-linked glycosylation and protein folding quality control. Through its role in co-translational glycan transfer, TUSC3 influences proteostasis, ER stress responses, and maturation of membrane and secreted proteins that feed into signaling and adhesion pathways. Altered TUSC3 expression or function has been associated with disrupted glycoprotein homeostasis and has been studied in contexts including cancer biology and neurodevelopmental phenotypes such as intellectual disability. These features make TUSC3 a useful node for investigating ER-associated processing, glycoprotein-dependent signaling, and stress adaptation mechanisms in human cells.

TUSC3 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 TUSC3 upregulation across a broader range of human cell types.

TUSC3 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 TUSC3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TUSC3 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native TUSC3 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.