ZEB Lentiviral Activation Particles (h): sc-400201-LAC

Human ZEB1 encodes the zinc finger E-box–binding homeobox protein ZEB, a DNA-binding transcription factor that represses epithelial gene programs and coordinates epithelial–mesenchymal transition (EMT). ZEB1 integrates signaling from pathways such as TGF-β/SMAD, WNT/β-catenin, and Notch, remodeling chromatin and altering cell adhesion, polarity, and motility through regulation of targets including CDH1 and other junctional components. Through these networks, ZEB1 contributes to lineage specification, developmental patterning, and stress-responsive transcriptional programs. Dysregulated ZEB1 activity and EMT-associated transcriptional states are frequently linked to invasion, stem-like phenotypes, and therapy resistance mechanisms studied across multiple disease models.

ZEB1 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 ZEB1 upregulation across a broader range of human cell types.

ZEB1 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 ZEB1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous ZEB1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native ZEB1 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.