Amphiregulin Lentiviral Activation Particles (h): sc-400987-LAC

AREG encodes amphiregulin, a secreted epidermal growth factor receptor (EGFR/ErbB1) ligand that is produced by epithelial cells, fibroblasts, and multiple immune subsets in response to injury and inflammatory cues. Upon binding EGFR, amphiregulin promotes receptor dimerization and activates downstream MAPK/ERK, PI3K/AKT, and JAK/STAT signaling, coordinating cell proliferation, survival, and tissue remodeling. AREG expression is commonly induced by cytokine- and stress-responsive transcriptional programs and contributes to paracrine signaling within local microenvironments. Dysregulated amphiregulin–EGFR signaling has been linked to pathological inflammation, fibrosis, and oncogenic processes, making AREG a relevant target for mechanistic studies of epithelial–stromal crosstalk and microenvironmental regulation.

Amphiregulin 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 AREG upregulation across a broader range of human cell types.

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