Estrogen Receptor beta Lentiviral Activation Particles (h): sc-400213-LAC

Human ESR2 encodes estrogen receptor beta (ERβ), a ligand-activated nuclear receptor that functions as a transcription factor regulating gene networks involved in cell differentiation, proliferation, apoptosis, inflammation, and metabolic homeostasis. Upon binding estrogens or selective ligands, ERβ engages canonical nuclear receptor signaling via estrogen response elements and crosstalk with MAPK/ERK, PI3K/AKT, NF-κB, and TGF-β pathways to shape context-specific transcriptional programs. ESR2 expression and ERβ activity have been implicated in hormone-responsive biology across reproductive, cardiovascular, immune, and central nervous system tissues, and are frequently studied for their roles in tumor biology, endocrine regulation, and inflammatory disease mechanisms. Dysregulated ESR2 signaling can alter chromatin-state-dependent transcription, making it a relevant target for investigating receptor isoforms, co-regulator usage, and pathway rewiring in disease-associated cellular models.

Estrogen Receptor beta 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 ESR2 upregulation across a broader range of human cell types.

Estrogen Receptor beta 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 ESR2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Estrogen Receptor beta expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native ESR2 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.