kinases (GRKs) and subsequent recruitment of β-arrestins, resulting in receptor internalization into endosomes has been extended by discovering that some internalized GPCRs continue to signal via G proteins from endosomes the parathyroid hormone (PTH) type 1 receptor (PTHR), which engages on sustained cAMP signaling from endosomes This mini-review discusses recent insights into the mechanisms of PTHR endosomal signaling and its physiological

protein complex in neurotransmitter release has been well characterized, the mechanisms that modulate the delivery molecular players, including SNARE proteins; here, SNARE proteins play a role in the fusion of recycling endosomes

GPCRs, G proteins, and arrestins on endosomal membranes3,4. Furthermore, targeting GPCRs in specific cellular compartments requires precise delivery mechanisms to This may involve the development of specialized delivery vehicles, such as nanoparticles or liposomes expressed in cellular compartments require innovative approaches to overcome barriers related to stability, delivery Towards a molecular understanding of endosomal trafficking by Retromer and Retriever.

She recently led a project that demonstrated the GPCR kinases (GRKs) can translocate to endosomes, and

signaling outputs of biased agonists, and demonstrating the ligand specificity behind GRK recruitment to endosomes

of the adaptor protein, β-arrestin, is a tag for receptor internalization and formation of signaling endosomes