G Protein-Coupled Receptors in Cell Signaling Transductions 2.0

Dear Colleagues,

This is a continued issue of our successful Special Issue “G Protein-Coupled Receptors in Cell Signaling Transduction”.

G protein-coupled receptors (GPCRs) and their downstream signaling pathways are critical targets for current pharmacotherapy. More than one-third of the drugs in use today act on GPCRs either as agonists, inverse agonists, or antagonists; however, their therapeutic potential is not exhausted, especially since recent findings point to new pharmacotherapeutically relevant regulatory mechanisms. In particular, hitherto largely unknown non-classical or, as they are also termed, non-canonical regulatory mechanisms of GPCR signaling have been identified that can either modulate canonical signaling by G proteins or trigger unrelated signaling events. These pathways are governed by receptor classes other than GPCRs, and various non-receptor regulators, including activators of G protein signaling (AGS) proteins or phosphate transferring nucleoside diphosphate kinases (NDPKs). GPCR adapters, such as arrestins and regulators of G protein signaling (RGS), can exert additional functions distinct from the inactivation of G protein signaling. Original research articles, reviews, and communications on the (patho)physiological relevance of canonical as well as non-canonical GPCR signaling in biological processes, such as tumor progression, autophagy, and cell movement, which are crucial for major human diseases, including cancer, metabolic disorders, cardiovascular diseases, immune responses, and (neuro-)sensory defects, will be particularly appreciated.

Prof. Dr. Sandra Beer-Hammer
Prof. Dr. Ines Liebscher
Guest Editors

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• GPCRs
• G-Proteins
• canonical/non-canonical signaling
• AGS proteins
• RGS proteins
• β-arrestin
• NDPKs
• pharmacological intervention
• biased ligands