ABCG2 Lentiviral Activation Particles (h): sc-416737-LAC

ABCG2 (also known as BCRP) is a human ATP-binding cassette (ABC) efflux transporter that exports a wide range of xenobiotics and endogenous metabolites across the plasma membrane. It contributes to barrier and detoxification functions in tissues such as intestine, liver, placenta, and the blood–brain barrier, and it helps regulate intracellular exposure to small molecules through ATP-dependent transport. ABCG2 activity intersects with cellular stress and metabolic homeostasis pathways by controlling porphyrin/heme-related metabolite handling and redox-associated substrate flux. Altered ABCG2 expression or function has been implicated in multidrug transport phenotypes in cancer biology and in inherited and acquired disorders of urate handling and gout risk via effects on urate transport.

ABCG2 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 ABCG2 upregulation across a broader range of human cell types.

ABCG2 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 ABCG2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous ABCG2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native ABCG2 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.