Graeme Milligan

TL;DR: The information on mechanisms responsible for signal bifurcation in G protein-linked receptors is analyzed and whether they are dependent upon either levels of expression of the receptor or the cell type is considered.

TL;DR: Differential pharmacology, function and regulation of GPCR hetero-dimers and -oligomers suggest means to selectively target GPCRs in different tissues and hint that the mechanism of function of several pharmacological agents might be different in vivo than anticipated from simple ligand-screening programmes that rely on heterologous expression of a single G PCR.

TL;DR: It is indicated that CXCR1-CXCR2 heterodimers are as likely to form in cells co-expressing these two chemokine receptors as the corresponding homodimer and stand in contrast to previous studies indicating an inability of the CX CR1 receptor to homodimerize or to interact with the C XCR2 receptor.

TL;DR: This work validate CRISPR/Cas9 engineered HEK293 cells lacking Gq/11 or arrestin2/3 as systems for GPCR signaling research and employ these cells to reveal a previously unappreciated interplay of signaling pathways where receptor phosphorylation can impact on ERK1/2 signaling through a mechanism that is likely independent of arrestins.

TL;DR: It is concluded that M1 muscarinic receptor inhibition of IK(M) is transduced by G alpha q and/or G alpha 11, and that G alpha o transduces alpha‐adrenoceptor inhibition of ICa.