GATA3 Lentiviral Activation Particles (h): sc-400134-LAC

GATA3 encodes a zinc-finger transcription factor that binds the GATA consensus motif to regulate lineage-specifying gene programs, with prominent roles in T-cell differentiation, epithelial development, and mammary gland biology. In immune cells, GATA3 functions as a key node in Th2 polarization by coordinating cytokine transcription and chromatin accessibility, integrating signals across JAK/STAT- and cytokine-driven transcriptional networks. In epithelial contexts it contributes to differentiation and maintenance of cell identity, influencing transcriptional circuits that intersect with hormone receptor signaling and developmental pathways. Dysregulated GATA3 activity or expression has been associated with altered immune responses and subtype-specific features of breast and other epithelial cancers, making it a widely used marker and mechanistic target for studying differentiation and transcriptional regulation.

GATA3 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 GATA3 upregulation across a broader range of human cell types.

GATA3 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 GATA3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous GATA3 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native GATA3 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.