GATA4 Lentiviral Activation Particles (h2): sc-400122-LAC-2

Human GATA4 encodes a zinc-finger transcription factor that binds GATA motifs to regulate gene programs controlling cardiac development, cardiomyocyte differentiation, and endoderm-derived organ formation, including liver and pancreas. GATA4 integrates with co-factors such as TBX5, NKX2-5, and FOG proteins to modulate enhancer activity and chromatin state within pathways governing morphogenesis, cell fate specification, and stress-responsive transcription in the heart. Genetic disruption or altered regulation of GATA4 is associated with congenital heart defects and has been linked to cardiac remodeling and select cancers through effects on lineage-specific transcriptional networks. Gene editing or perturbation of GATA4 is widely used to dissect enhancer function, model developmental phenotypes in iPSC-derived lineages, and map transcriptional circuitry by combining knockout/knock-in strategies with RNA-seq and epigenomic profiling.

GATA4 Lentiviral Activation Particles (h2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient GATA4 upregulation across a broader range of human cell types.

GATA4 Lentiviral Activation Particles (h2) 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 GATA4 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous GATA4 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native GATA4 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.