ETAR Lentiviral Activation Particles (h): sc-401000-LAC

EDNRA encodes endothelin receptor type A (ETAR), a G protein–coupled receptor that binds endothelin-1 to regulate vascular smooth muscle contraction and broader cardiovascular homeostasis. Upon ligand engagement, ETAR primarily signals through Gαq/11 to activate phospholipase C, elevating intracellular Ca2+ and stimulating PKC, with additional coupling to MAPK/ERK and RhoA/ROCK pathways that influence proliferation, migration, and extracellular matrix remodeling. EDNRA-driven signaling also interfaces with inflammatory and hypoxia-associated programs that modulate endothelial–smooth muscle communication. Dysregulated ETAR activity and endothelin axis imbalance are implicated in vascular dysfunction and remodeling contexts, supporting its use as a mechanistic node for pathway interrogation in relevant cellular models.

ETAR 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 EDNRA upregulation across a broader range of human cell types.

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