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- W4313491569 endingPage "102347" @default.
- W4313491569 startingPage "102347" @default.
- W4313491569 abstract "Store-Operated Ca2+ entry (SOCE) is recognized as a key mechanism in muscle physiology necessary to refill intracellular Ca2+ stores during sustained muscle activity. For many years the cell structures expected to mediate SOCE in skeletal muscle fibres remained unknown. Recently, the identification of Ca2+ Entry Units (CEUs) in exercised muscle fibres opened new insights into the role of extracellular Ca2+ in muscle contraction and, more generally, in intracellular Ca2+ homeostasis. Accordingly, intracellular Ca2+ unbalance due to alterations in SOCE strictly correlates with muscle disfunction and disease. Mutations in proteins involved in SOCE (STIM1, ORAI1, and CASQ1) have been linked to tubular aggregate myopathy (TAM), a disease that causes muscle weakness and myalgia and is characterized by a typical accumulation of highly ordered and packed membrane tubules originated from the sarcoplasmic reticulum (SR). Achieving a full understanding of the molecular pathways activated by alterations in Ca2+ entry mechanisms is a necessary step to design effective therapies for human SOCE-related disorders." @default.
- W4313491569 created "2023-01-06" @default.
- W4313491569 creator A5031271799 @default.
- W4313491569 creator A5032282263 @default.
- W4313491569 creator A5070423090 @default.
- W4313491569 creator A5071586379 @default.
- W4313491569 date "2023-02-01" @default.
- W4313491569 modified "2023-10-14" @default.
- W4313491569 title "Store-operated calcium entry: From physiology to tubular aggregate myopathy" @default.
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