ErbB2/HER2 Lentiviral Activation Particles (h): sc-400138-LAC

ERBB2 encodes the receptor tyrosine kinase ErbB2/HER2, a ligand-orphan member of the EGFR/ErbB family that functions as a preferred heterodimerization partner to amplify growth factor signaling. Upon dimerization, HER2 activates downstream PI3K–AKT–mTOR and RAS–RAF–MEK–ERK cascades, coordinating proliferation, survival, differentiation, and metabolic programs. ERBB2 signaling also interfaces with SRC/FAK and cell–cell adhesion networks, influencing cytoskeletal dynamics and migratory behavior. Dysregulated ERBB2 expression or pathway hyperactivation is strongly associated with oncogenic transformation and is widely studied as a driver of tumor cell fitness and signaling plasticity in multiple tissue contexts.

ErbB2/HER2 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 ERBB2 upregulation across a broader range of human cell types.

ErbB2/HER2 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 ERBB2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous ErbB2/HER2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native ERBB2 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.