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Structure andRegulation ofVoltage-Gated Ca2+Channels William A. Catterall2000 год

Structure and Regulation of Voltage-Gated Ca2+ Channels
review

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Аннотация: ▪ Abstract Voltage-gated Ca 2+ channels mediate Ca 2+ entry into cells in response to membrane depolarization. Electrophysiological studies reveal different Ca 2+ currents designated L-, N-, P-, Q-, R-, and T-type. The high-voltage-activated Ca 2+ channels that have been characterized biochemically are complexes of a pore-forming α 1 subunit of ∼190–250 kDa; a transmembrane, disulfide-linked complex of α 2 and δ subunits; an intracellular β subunit; and in some cases a transmembrane γ subunit. Ten α 1 subunits, four α 2 δ complexes, four β subunits, and two γ subunits are known. The Ca v 1 family of α 1 subunits conduct L-type Ca 2+ currents, which initiate muscle contraction, endocrine secretion, and gene transcription, and are regulated primarily by second messenger-activated protein phosphorylation pathways. The Ca v 2 family of α 1 subunits conduct N-type, P/Q-type, and R-type Ca 2+ currents, which initiate rapid synaptic transmission and are regulated primarily by direct interaction with G proteins and SNARE proteins and secondarily by protein phosphorylation. The Ca v 3 family of α 1 subunits conduct T-type Ca 2+ currents, which are activated and inactivated more rapidly and at more negative membrane potentials than other Ca 2+ current types. The distinct structures and patterns of regulation of these three families of Ca 2+ channels provide a flexible array of Ca 2+ entry pathways in response to changes in membrane potential and a range of possibilities for regulation of Ca 2+ entry by second messenger pathways and interacting proteins.
Год издания: 2000
Авторы: William A. Catterall
Издательство: Annual Reviews
Источник: Annual Review of Cell and Developmental Biology
Ключевые слова: Ion channel regulation and function, Neuroscience and Neural Engineering, Cardiac electrophysiology and arrhythmias
Другие ссылки: Annual Review of Cell and Developmental Biology (HTML)
PubMed (HTML)