NOS2/iNOS Lentiviral Activation Particles (h): sc-400066-LAC

Human NOS2 encodes inducible nitric oxide synthase (iNOS), a high-output enzyme that converts L-arginine to nitric oxide and L-citrulline in response to inflammatory cues. NOS2/iNOS is transcriptionally regulated downstream of NF-κB, JAK/STAT, and MAPK signaling, integrating cytokine and microbial pattern–driven pathways to shape innate immunity, redox balance, and antimicrobial effector functions. Sustained iNOS activity modulates nitrosative stress, protein S-nitrosylation, and mitochondrial function, with downstream effects on apoptosis, angiogenic signaling, and extracellular matrix remodeling. Dysregulated NOS2 expression has been associated with chronic inflammation and tumor microenvironment biology, making it a widely used target for mechanistic studies in immunology, neuroinflammation, and cancer-related signaling.

NOS2/iNOS 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 NOS2 upregulation across a broader range of human cell types.

NOS2/iNOS 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 NOS2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous NOS2/iNOS expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native NOS2 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.