AHRR Lentiviral Activation Particles (h): sc-412812-LAC

Human AHRR (aryl-hydrocarbon receptor repressor) encodes a ligand-inducible transcriptional repressor that provides negative feedback control over AHR-dependent gene expression. AHRR competes with AHR for ARNT and binds xenobiotic response elements to attenuate transcription of detoxification and stress-response programs, shaping cellular responses to environmental ligands and endogenous metabolites. Through modulation of CYP enzyme networks, oxidative stress signaling, and inflammatory gene regulation, AHRR influences epithelial barrier function, immune polarization, and metabolic homeostasis. Altered AHRR activity or expression has been linked to dysregulated xenobiotic signaling and is frequently studied in contexts including carcinogenesis, airway disease, and immune-mediated inflammation.

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

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