TRB-3 Lentiviral Activation Particles (h): sc-401746-LAC

TRIB3 encodes tribbles pseudokinase 3 (TRB-3), a catalytically inactive kinase-like adaptor that modulates signal transduction by scaffolding protein–protein interactions. TRB-3 is best known for negatively regulating the PI3K/AKT axis through interaction with AKT, thereby influencing insulin signaling, cellular metabolism, and stress-adaptive programs. It also integrates endoplasmic reticulum stress responses and can intersect with MAPK and TGF-β/SMAD-related pathways to shape cell survival, differentiation, and inflammatory signaling. Dysregulated TRIB3 expression has been associated with metabolic dysfunction, cardiovascular and neurodegenerative processes, and cancer-relevant phenotypes such as altered apoptosis and therapy stress tolerance, making it a useful node for pathway-focused mechanistic studies.

TRB-3 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 TRIB3 upregulation across a broader range of human cell types.

TRB-3 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 TRIB3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TRB-3 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native TRIB3 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.