Figure 1.

Three major processes implicated in Ca²⁺ signal stimulus-induced dynamic alterations: encoding, decoding and retaining. Ca²⁺ encoding is mediated by Ca²⁺ channels, Ca²⁺-ATPases, Ca²⁺/H⁺ exchangers, channels named CNGCs, GLRs, TPCs, MCAs, MSLs, OSCA1, ATPases named ACAs, ECAs, and the antiporter named CAX; besides this, annexins without EF-hand domains are also involved in Ca²⁺ influx. The decoding is composed of many different protein families. CaMs, CMLs and CBLs harbor EF hand domains and regulate target proteins without any additional functional domains. CBLs modulate the activity of CIPKs interacting with NAF and PPI domain, while CDPKs are directly activated by Ca²⁺ binding to the CaM-like domain. In contrast to CDPKs, CCaMKs are dual-regulated kinases. These proteins bind Ca²⁺ via a visinin-like domain, while in addition, Ca²⁺-CaM binds to the regulatory domain of the kinase and mediates further activation. CAMTAs activate the transcription of related genes by interacting with CaM. Ca²⁺ signatures retain a steady-state concentration under the same stimulation for a short period through persistent decaying or during a refractory period. Colored modules represent different functional structures. The black lines with an arrow indicate the direction of Ca²⁺ flow, and the black curve with an arrow indicates the ATP decomposition reaction (ATP to ADP).