GPCRsignalen

GPCRsignalen refers to the cellular signaling processes initiated by G protein-coupled receptors (GPCRs), a large and diverse family of cell-surface receptors characterized by seven transmembrane helices. When an extracellular ligand binds, the receptor undergoes a conformational change that promotes exchange of GDP for GTP on the Gα subunit of a heterotrimeric G protein, triggering dissociation of Gα-GTP from Gβγ.

Both types of subunits then regulate various effector proteins to generate second messengers such as cyclic AMP, inositol trisphosphate (IP3), diacylglycerol (DAG), and calcium ions, ultimately producing specific cellular responses. GPCRsignalen pathways are broadly categorized by Gα subunits: Gs stimulates adenylyl cyclase increasing cAMP; Gi/o inhibits it; Gq/11 activates phospholipase Cβ, producing IP3 and DAG and increasing intracellular Ca2+.

Additional regulation occurs via ion channels and kinase cascades, and through beta-arrestins which mediate desensitization and can initiate G protein-independent signaling. GPCR signaling is tightly regulated by receptor phosphorylation, endocytosis, recycling, and degradation.

Physiological roles are extensive, including vision, olfaction, taste, heart rate control, neurotransmission, and hormonal signaling. Pharmacology heavily targets GPCRs; many therapeutics operate as agonists, antagonists, or allosteric modulators. The concept of biased agonism highlights that some ligands preferentially evoke G protein or beta-arrestin pathways, offering therapeutic potential with reduced side effects.

GPCRsignalen exemplifies a central mechanism in cell communication, integrating extracellular cues with intracellular responses across tissues and systems.