Androgen Receptor Lentiviral Activation Particles (h): sc-400026-LAC

Human AR encodes the androgen receptor, a ligand-activated nuclear hormone receptor that functions as a transcription factor controlling genes involved in sexual differentiation, reproductive biology, and tissue-specific growth programs. Upon androgen binding, AR undergoes conformational activation, nuclear translocation, and DNA binding at androgen response elements to regulate chromatin state and transcription through co-regulator recruitment. AR signaling intersects with PI3K–AKT, MAPK, and cell-cycle regulatory networks, shaping proliferation, differentiation, and metabolic homeostasis. Dysregulated AR expression or signaling is implicated in hormone-driven pathophysiology and is widely studied as a molecular determinant of lineage state and transcriptional plasticity in androgen-responsive tissues.

Androgen Receptor 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 AR upregulation across a broader range of human cell types.

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