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.

Two modes of GPCR endocytosis by β-arrestin are differentially coupled to downstream signaling.

The vasopressin type 2 receptor promotes dual Gα_s and Gα_q/11 signaling at early endosomes in β-arrestin-dependent and -independent manners.

Phosphoproteomics identifies β-arrestin 2 phosphorylation at Thr383 by MEK as a key step of GPCR-induced Erk½ activation, thus providing new insight into the molecular mechanism underlying β-arrestin-dependent GPCR-operated signaling.

Systematic CRISPR-based editing of tRNA genes revealed that different human cells that span a range of growth rates and different modes of proliferation states require diverse tRNA sets.

Unveiling the high-confidence protein–protein interaction networks of human and fly α-arrestins provides insights into conserved and species-specific functional roles depending on their protein domains and motifs.

β-arrestins recruit Nedd4 ubiquitin E3 ligase to mGlu7 receptor and facilitate ubiquitination, endocytosis, ERK signaling, and stability of mGlu7 at presynaptic terminals.

Biallelic MAD2L1BP variants contribute to oocyte metaphase I arrest in women with primary infertility and p31^comet is required for human oocyte maturation.

The key mechanism for opioid-like biased agonists to provide analgesia but not respiratory depression does not involve ß-arrestin 2.

Ligand-specific-induced conformations of M₃ muscarinic receptors reveal similar requirements for G protein-coupled receptor kinase 2 and G_q protein binding, whereas arrestin3 binding is mediated by distinct receptor conformations.