CD47 Lentiviral Activation Particles (h): sc-400508-LAC

Human CD47 encodes an immunoglobulin superfamily transmembrane protein that functions as a key “self” recognition signal through its interaction with SIRPα on myeloid cells, modulating phagocytosis and innate immune surveillance. CD47 also binds thrombospondin-1, influencing cell adhesion, migration, nitric oxide signaling, and vascular and inflammatory responses. Through these receptor–ligand interactions, CD47 integrates cytoskeletal remodeling and survival signaling with tissue homeostasis. Dysregulated CD47 expression has been associated with tumor immune evasion phenotypes and altered inflammatory and vascular biology, making it relevant for mechanistic studies of immune regulation and microenvironmental signaling.

CD47 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 CD47 upregulation across a broader range of human cell types.

CD47 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 CD47 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CD47 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native CD47 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.