Stat3 Lentiviral Activation Particles (h): sc-400027-LAC

Human STAT3 encodes Stat3, a latent cytoplasmic transcription factor activated by cytokine and growth factor signaling. Following phosphorylation downstream of JAK kinases and receptor tyrosine kinases, Stat3 dimerizes and translocates to the nucleus to regulate programs controlling proliferation, survival, inflammation, and differentiation, including acute-phase and immune modulatory genes. STAT3 integrates signals from pathways such as IL-6/GP130–JAK–STAT, EGFR, and crosstalk with NF-κB and PI3K/AKT. Dysregulated STAT3 activity is frequently associated with altered immune signaling, chronic inflammatory states, and oncogenic transcriptional networks, making it a common node for mechanistic studies of signal transduction and gene regulation.

Stat3 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 STAT3 upregulation across a broader range of human cell types.

Stat3 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 STAT3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Stat3 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native STAT3 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.