CD39 Lentiviral Activation Particles (m): sc-419549-LAC

Entpd1 encodes the ectonucleotidase CD39 (ENTPD1), a cell-surface enzyme that hydrolyzes extracellular ATP and ADP to AMP, shaping purinergic signaling in vascular, immune, and stromal compartments in mouse. By regulating nucleotide availability, CD39 influences inflammatory signaling, platelet and endothelial responses, and the balance between ATP-driven danger cues and adenosine-generating immunoregulatory pathways in concert with CD73. CD39 activity is linked to modulation of leukocyte activation, cytokine production, and tissue injury responses, making Entpd1 a relevant target in models of inflammation, thrombosis, ischemia-reperfusion injury, and tumor-associated immune regulation. Its expression is commonly studied on regulatory T cells, myeloid populations, and endothelium where extracellular nucleotide metabolism controls cell–cell communication.

CD39 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 Entpd1 upregulation across a broader range of human cell types.

CD39 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 Entpd1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CD39 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Entpd1 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.