Ah Receptor Lentiviral Activation Particles (m): sc-419054-LAC

Mouse Ahr encodes the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor that functions as a central environmental sensor linking xenobiotic exposure to transcriptional reprogramming. Upon activation, AhR translocates to the nucleus, heterodimerizes with ARNT, and binds xenobiotic response elements to regulate genes involved in phase I/II metabolism such as cytochrome P450 enzymes, intersecting with oxidative stress and inflammatory signaling pathways. Beyond detoxification, AhR influences immune cell differentiation, epithelial barrier maintenance, and developmental processes through crosstalk with NF-κB, Wnt/β-catenin, and circadian regulatory networks. Dysregulated AhR signaling has been implicated in toxicological responses and inflammatory phenotypes, and it is frequently studied in contexts such as barrier dysfunction, immune-mediated pathology, and carcinogenesis-associated transcriptional programs.

Ah Receptor Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Ahr upregulation across a broader range of human cell types.

Ah Receptor Lentiviral Activation Particles (m) 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 Ahr transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Ah Receptor expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Ahr 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.