CD274/PD-L1 Lentiviral Activation Particles (m): sc-425636-LAC

Cd274 encodes CD274/PD-L1, an immune checkpoint ligand that binds PD-1 on activated T cells and modulates downstream signaling to dampen TCR-driven activation, cytokine production, and cytotoxic effector function. In mice, PD-L1 expression is dynamically regulated by inflammatory cues such as IFN-γ through JAK/STAT pathways and intersects with antigen presentation and interferon-stimulated gene programs. CD274 contributes to peripheral tolerance and shapes immune cell–tumor and immune cell–stromal interactions by limiting excessive immune activation. Dysregulated PD-L1 is frequently studied in contexts of chronic inflammation, infection, autoimmunity models, and tumor immunology to understand mechanisms of immune evasion and adaptive resistance signaling.

CD274/PD-L1 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 Cd274 upregulation across a broader range of human cell types.

CD274/PD-L1 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 Cd274 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CD274/PD-L1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Cd274 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.