Adenosine A2A-R Lentiviral Activation Particles (h): sc-400807-LAC

ADORA2A encodes the human adenosine A2A receptor (A2A-R), a G protein–coupled receptor that primarily signals through Gs to elevate cAMP and activate PKA- and CREB-dependent transcriptional programs. A2A-R integrates extracellular adenosine cues with neuromodulatory and immunoregulatory circuits, shaping processes such as neurotransmitter release, synaptic plasticity, and inflammatory mediator production. Receptor activity intersects with MAPK/ERK signaling, calcium homeostasis, and regulation of cytokine networks, linking ADORA2A expression to stress responses and tissue microenvironmental changes. Dysregulated ADORA2A signaling has been studied in contexts including neuroinflammation, neurodegeneration, and tumor-associated immune suppression, making it relevant for pathway mapping and mechanistic target validation in human cell models.

Adenosine A2A-R 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 ADORA2A upregulation across a broader range of human cell types.

Adenosine A2A-R 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 ADORA2A transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Adenosine A2A-R expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native ADORA2A 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.