DRiP78 participates in the formation of receptor dimers, and contributes to the assembly of the G protein with the receptor into a complex. Previous studies demonstrated the interaction of Gbc with the receptor in the ER, while the interaction with the Ga subunit occurred outside of the ER, but before reaching the Golgi. Our results are in agreement with those from that study, since we show that DRiP78 alters the interaction between CCR5 and Ga. The incapacity of the receptor to leave the ER could explain this result. Whether the regulation of the assembly happens by a direct modulation signaling assembly or by favoring the interaction through retention in the same compartment remains to be determined. An increasing number of studies have shown that maturation and/or targeting of receptor oligomers to the cell surface are associated with human diseases. Chemokine receptors such as CCR5 demonstrate polymorphisms that induce significant changes in signaling capacities. For example, the CCR5D32 mutation retains the receptor intracellularly and confers significant levels of resistance to HIV infection. Retaining the CCR5 receptor has beneficial effects in the prevention of HIV infection. A better knowledge of the molecular mechanisms controlling receptor assembly could help understand how misfolded, polymorphic or mistrafficked receptors influence receptor complex cell surface expression and signal transduction. Over the last three decades, transgenic mice have become a mainstay of biological research, particularly for studies of gene expression and genetic gain of function experiments. With transgenes for experimental monitoring and manipulation, as well as CRE-mediated cell specific genetic modification. However, as experimental designs become more sophisticated, involving multiple alleles and distinct mouse backgrounds, breeding paradigms become severely rate limiting. Currently, most studies tend to utilize at most two alleles. A consideration of simple mendelian rules highlights the reason: the allele problem. To combine three or more alleles is time-consuming, inefficient, and wasteful of animal lives and experimental resources; only one animal in eight from heterozygote matings would carry all three transgenes and thus be of use for experimental applications. Likewise, traditional longitudinal anatomical studies, such as those for development or Rapamycin 53123-88-9 neural repair applications, require the sacrifice of a number of research animals for each time point and condition of interest. Technical advances in microscopy now permit relatively non-invasive in vivo longitudinal monitoring of cellular anatomy and activity, provided those cells are somehow labeled with appropriate fluorophores. However, most existing transgenic mouse lines only label one particular cell type, precluding studies entailing cellular interactions, or more comprehensive monitoring of ongoing processes. Ideally, one would be able to generate mouse lines where multiple transgenes have been inserted into a single locus, yet where each transgene maintains independent regulation in distinct cell types.