
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GATA3 Lentiviral Activation Particles (m) | sc-420495-LAC | 200 µl | $455.00 |
Mouse Gata3 encodes GATA3, a zinc-finger transcription factor that binds GATA motifs to control lineage-specific gene programs during embryogenesis and immune development. In hematopoietic cells, GATA3 is a central regulator of T cell differentiation, including Th2 polarization, and coordinates cytokine and receptor expression through enhancer remodeling and chromatin accessibility changes. GATA3 also contributes to epithelial differentiation and barrier function, linking transcriptional control to developmental signaling and tissue homeostasis. Dysregulated GATA3-dependent transcriptional networks are used as mechanistic models for immune imbalance, inflammatory phenotypes, and context-dependent oncogenic or tumor-suppressive programs in mouse systems.
GATA3 Lentiviral Activation Particles (m) 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 (m) 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.