A new form of chemokine signaling bias that depends on cell state is identified.

siRNA knockdown experiments reveal in detail the signaling pathway that controls cytoskeletal function during cell-in-cell invasion.

A unique two-step mechanism of plasma membrane recruitment and activation governs G-protein-coupled receptor mediated PI3K signaling.

Contrary to previous findings, class A GPCRs share a common activation pathway that directly links ligand binding to G-protein activation, as revealed by novel quantitative analysis.

MRGPRX4 is a bilirubin receptor that may be a therapeutic target for patients suffering from cholestatic itch.

Under normal nutritional conditions, G-protein coupled receptors can control autophagy by regulating the degradation of key autophagic regulator Atg14L through ZBTB16-mediated ubiquitination and proteasome degradation.

PTEN organizes multicellular architecture by non-catalytic scaffolding of spatially localized β-Arrestin1/ARHGAP21/Cdc42 protein complexes to control mitotic spindle orientation, multicellular configuration and lumen formation.

The cryo-EM structure of ET_B-G_i complex, obtained using the Fusion-G system, provides insights into the distinct activation mechanism and G-protein promiscuity of ET_B, aiding in the design of ET_B agonists for therapeutic applications.

The GPCR-G protein coupling map and selectivity insights will catalyze advances in receptor research, cellular signaling, and drug discovery exploiting G protein signaling bias to design safer drugs.