adenosine deaminase Lentiviral Activation Particles (h): sc-402201-LAC

Human ADA encodes adenosine deaminase, a key enzyme of purine metabolism that irreversibly deaminates adenosine and deoxyadenosine to inosine and deoxyinosine, thereby regulating intracellular and extracellular adenosine pools. By controlling the balance of nucleosides that influence DNA synthesis, energy homeostasis, and signaling through adenosine receptor pathways, ADA contributes to lymphocyte development and broader immune cell function. Dysregulated ADA activity perturbs purine catabolism and can alter nucleotide turnover, redox balance, and inflammatory signaling programs. ADA is therefore widely studied in models of immunodeficiency, immune activation, and metabolic stress where purine flux and adenosine-mediated signaling are central variables.

adenosine deaminase 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 ADA upregulation across a broader range of human cell types.

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