RFX6 Lentiviral Activation Particles (h2): sc-408496-LAC-2

Human RFX6 (regulatory factor X6) encodes a winged-helix transcription factor that binds X-box DNA motifs to control gene programs required for pancreatic endocrine lineage specification and the maturation and maintenance of insulin-producing β cells. It functions within transcriptional networks governing islet development, glucose-stimulated hormone secretion, and broader gene regulatory pathways that coordinate endoderm-derived cell fate decisions. Genetic disruption or dysregulated expression of RFX6 has been linked to congenital endocrine pancreas defects and forms of diabetes, making it a key node for studying monogenic diabetes mechanisms and islet cell dysfunction. Gene editing of RFX6 supports mechanistic interrogation of enhancer–promoter regulation, chromatin occupancy, and downstream endocrine gene circuits in human stem-cell differentiation models and pancreatic islet-relevant systems.

RFX6 Lentiviral Activation Particles (h2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient RFX6 upregulation across a broader range of human cell types.

RFX6 Lentiviral Activation Particles (h2) 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 RFX6 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous RFX6 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native RFX6 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.