Human UBC-RGS2-mCherry adenoviral particles

The human UBC-RGS2-mCherry adenovirus particles integrate the widely expressed human UBC promoter, a functional human RGS2 open reading frame, and an mCherry fluorescent tag into a replication-deficient adenovirus backbone, enabling reliable and traceable expression in a variety of cell types. These particles are constructed based on a standard E1/E3-deleted Ad5-derived system, exhibiting high transduction efficiency in both dividing and non-dividing cells, supporting robust but transient expression without genomic integration. The fused or co-expressed mCherry allows for direct visualization of expression, subcellular localization, and relative abundance in live or fixed samples using standard red fluorescence channels, facilitating experimental quality control and downstream quantitative analysis. RGS2, a key regulator of G protein signaling, particularly in the Gαq-coupled pathway, provides a mechanistically relevant payload for studying GPCR signal termination, calcium mobilization, and downstream effectors.

These particles are highly suitable for cardiovascular, neurological, and cell signaling research, where precise regulation of GPCR pathways is crucial. In the cardiovascular system, RGS2 is involved in vascular tone, endothelial function, and hypertrophic signaling. Delivering the adenovirus to primary vascular smooth muscle cells, endothelial cells, or cardiomyocytes can help model how enhanced RGS2 activity inhibits Gq/PLCβ signaling, affects calcium dynamics, or regulates MAPK cascades related to blood pressure and remodeling. In neurobiology, this construct supports studies of synaptic transmission, neuronal excitability, and stress circuits by attenuating hyperactive GPCR input and utilizing mCherry to visualize protein localization in dendrites, soma, or axons. In oncology and pharmacology, it can be used for pathway dissection, studying the role of GPCRs in cell proliferation, migration, or therapeutic resistance, and can serve as a readout platform for evaluating biased agonists or modulators acting on the Gq pathway.