Ep-CAM Lentiviral Activation Particles (m): sc-421499-LAC

Mouse Epcam encodes Ep-CAM, a transmembrane glycoprotein enriched at epithelial cell–cell contacts that contributes to adhesion, epithelial polarity, and barrier organization. Ep-CAM interfaces with junctional and cytoskeletal remodeling programs and is linked to proliferative signaling networks, including pathways that coordinate epithelial homeostasis and stem-like cell states. Altered EPCAM expression is frequently used as a marker of epithelial lineage and phenotypic transitions, including changes associated with invasion and differentiation status in cancer biology. In mouse models, Epcam is widely studied in development, tissue regeneration, and epithelial-derived tumor systems to understand how adhesion-linked signaling shapes cellular identity.

Ep-CAM 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 Epcam upregulation across a broader range of human cell types.

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