EGFR Lentiviral Activation Particles (h): sc-400015-LAC

Epidermal growth factor receptor (EGFR) is a human receptor tyrosine kinase that regulates epithelial cell proliferation, survival, migration, and differentiation through ligand-induced dimerization and autophosphorylation. Activated EGFR engages core signaling cascades including RAS–RAF–MEK–ERK, PI3K–AKT–mTOR, JAK–STAT, and PLCγ–PKC, coordinating transcriptional programs and cell-cycle control. Tight regulation of EGFR abundance and activity is maintained by endocytosis, ubiquitination, and feedback inhibition to balance growth cues with tissue homeostasis. Dysregulated EGFR signaling and expression are widely studied in oncogenic transformation, invasion, and therapy resistance mechanisms, and EGFR also contributes to wound repair and inflammatory signaling in diverse cell contexts.

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

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