TRAF6 Lentiviral Activation Particles (h): sc-400117-LAC

TRAF6 (TNF receptor–associated factor 6) is an E3 ubiquitin ligase and adaptor protein that couples upstream receptors to downstream signaling in innate immunity and inflammation. It mediates K63-linked polyubiquitination to activate TAK1 and the IKK complex, driving NF-κB and MAPK (JNK/p38) pathways, and it also interfaces with IRF-dependent responses in select contexts. TRAF6 functions downstream of Toll-like receptors, IL-1 receptor family members, and RANK, influencing cytokine production, osteoclast differentiation, and cell survival programs. Dysregulated TRAF6 signaling has been associated with chronic inflammatory states, autoimmune phenotypes, bone remodeling defects, and oncogenic signaling networks in multiple tumor types.

TRAF6 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 TRAF6 upregulation across a broader range of human cell types.

TRAF6 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 TRAF6 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TRAF6 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native TRAF6 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.