Nur77 Lentiviral Activation Particles (h): sc-418320-LAC

Human NR4A1 encodes Nur77, an immediate-early orphan nuclear receptor that functions as a ligand-responsive transcription factor linking stimulus-dependent signaling to rapid gene expression programs. Nur77 integrates cues from MAPK, NF-κB, and calcium-dependent pathways to regulate immune activation and tolerance, apoptosis and mitochondrial stress responses, and metabolic adaptation. In lymphocytes and myeloid cells, NR4A1 influences T cell anergy/exhaustion phenotypes and inflammatory cytokine networks, while in other contexts it modulates cell-cycle control and stress-induced transcription. Dysregulated NR4A1/Nur77 activity has been associated with chronic inflammation, autoimmunity, and cancer-relevant transcriptional remodeling, making it a useful node for mechanistic studies of signaling-to-transcription coupling.

Nur77 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 NR4A1 upregulation across a broader range of human cell types.

Nur77 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 NR4A1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Nur77 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native NR4A1 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.