Gproteinkaskad

G proteinkaskad, or G protein cascade, refers to a set of signal transduction pathways in which signals received at the cell surface are transmitted through heterotrimeric G proteins linked to G protein-coupled receptors (GPCRs). These cascades convert extracellular cues into intracellular responses that regulate processes such as metabolism, secretion, movement, and gene expression.

Mechanism begins when a ligand binds a GPCR, promoting exchange of GDP for GTP on the G alpha subunit of the heterotrimer. The GTP-bound G alpha dissociates from the G beta-gamma dimer, and both components can regulate downstream effectors at the plasma membrane. Common targets include adenylyl cyclase, which raises cAMP; phospholipase C-beta, which produces IP3 and DAG leading to calcium release and PKC activation; and various ion channels. Through these routes, a single signal can be amplified to elicit broad cellular responses. G protein families include Gs (stimulatory, increases cAMP), Gi (inhibitory, decreases cAMP), and Gq (activates PLC-beta).

Signal termination involves the intrinsic GTPase activity of G alpha, often accelerated by regulators of G protein signaling (RGS proteins). Receptor desensitization can occur via GPCR kinases (GRKs) and arrestins, reducing signaling. Spatial organization and scaffold proteins also shape responses and limit cross-talk with other pathways.

Examples include beta-adrenergic signaling in the heart (Gs-coupled, elevating cAMP) and visual signaling in the retina (Gt/transducin). The gproteinkaskad is essential for physiological control of metabolism, secretion, sensory perception, and development, and it is a major target for pharmacological intervention. Dysregulation of GPCR–G protein signaling is linked to various diseases, including hypertension and obesity.