CaMKWege

CaMKWege is a term sometimes used in neuroscience and cell signaling to describe the network of pathways governed by calcium/calmodulin-dependent protein kinases (CaMKs). The concept emphasizes how CaMKs translate intracellular calcium fluctuations into a broad range of cellular responses, and how different CaMK family members coordinate within signaling cascades.

The CaMK family includes CaMKII, CaMKIV, CaMKI, and the upstream activator CaMKK. Upon rises in intracellular Ca2+, calmodulin binds calcium and activates these kinases. CaMKII is notable for its multimeric holoenzyme structure and its Autophosphorylation at threonine 286, which can confer autonomous activity beyond Ca2+ signals. CaMKK can activate CaMKI and CaMKIV, linking calcium signals to gene regulation and metabolic control. Activation and inactivation are further modulated by phosphatases, scaffold proteins, and subcellular localization, creating a diverse set of signaling outputs across tissues.

Representative CaMKWege outputs include regulation of synaptic plasticity through AMPA receptor trafficking and spine remodeling (primarily by CaMKII), modulation of gene expression via CREB phosphorylation (often involving CaMKIV), and metabolic or transcriptional changes through CaMKK-activated pathways such as AMPK. In cardiac and other muscle cells, CaMKII affects calcium handling and contractility by targeting calcium-handling proteins, illustrating tissue-specific branches of the same signaling network.

The term CaMKWege is not uniformly standardized and is used mainly to discuss the integrated, network-like nature of CaMK signaling. For precise mechanisms, researchers typically refer to individual CaMK pathways and their specific substrates. See also calcium signaling, calmodulin, CaMKII, CREB, and synaptic plasticity.