Stat1 Lentiviral Activation Particles (h): sc-400086-LAC

Human STAT1 encodes Stat1, a central transcription factor in interferon and cytokine signaling that transduces signals downstream of type I, II, and III interferon receptors through the JAK–STAT pathway. Upon phosphorylation, Stat1 dimerizes and accumulates in the nucleus to regulate interferon-stimulated genes involved in antiviral defense, antigen presentation, apoptosis, and control of cell proliferation. STAT1 activity also intersects with innate immune pathways such as pattern recognition receptor signaling and NF-κB–dependent inflammatory programs, shaping macrophage and T cell responses. Dysregulated STAT1 signaling has been linked to altered host defense and immune homeostasis and is frequently studied in the context of infectious disease biology, inflammation, and tumor–immune interactions.

Stat1 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 STAT1 upregulation across a broader range of human cell types.

Stat1 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 STAT1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Stat1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native STAT1 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.