FOXP3 Lentiviral Activation Particles (h): sc-400542-LAC

FOXP3 encodes a forkhead/winged-helix transcription factor that serves as a master regulator of regulatory T cell (Treg) lineage commitment and suppressive function. By coordinating transcriptional programs that modulate cytokine signaling, T cell receptor-driven activation, and immune checkpoint pathways, FOXP3 helps maintain peripheral immune tolerance and restrain excessive inflammation. Dysregulated FOXP3 expression or activity is linked to impaired Treg stability and aberrant immune responses, making it a central node for studying immune homeostasis. FOXP3 is also used as a molecular marker in immunology research to interrogate Treg differentiation, chromatin-state remodeling, and inflammatory disease-associated transcriptional networks.

FOXP3 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 FOXP3 upregulation across a broader range of human cell types.

FOXP3 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 FOXP3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous FOXP3 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native FOXP3 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.