Document Detail


What role for store-operated Ca²⁺ entry in muscle?
MedLine Citation:
PMID:  23312019     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Store-operated Ca²⁺ entry (SOCE) is a receptor-regulated Ca²⁺ entry pathway that is both ubiquitous and evolutionarily conserved. SOCE is activated by depletion of intracellular Ca²⁺ stores through receptor-mediated production of inositol 1,4,5-trisphosphate (IP₃). The depletion of endoplasmic reticulum (ER) Ca²⁺ is sensed by stromal interaction molecule 1 (STIM1). On store depletion, STIM1 aggregates and moves to areas where the ER comes close to the plasma membrane (PM; within 25 nm) to interact with Orai1 channels and activate Ca²⁺ entry. Ca²⁺ entry through store-operated Ca²⁺ (SOC) channels, originally thought to mediate the replenishment of Ca²⁺ stores, participate in active downstream signaling by coupling to the activation of enzymes and transcription factors that control a wide variety of long-term cell functions such as proliferation, growth, and migration. SOCE has also been proposed to contribute to short-term cellular responses such as muscle contractility. While there are significant STIM1/Orai1 protein levels and SOCE activity in adult skeletal muscle, the precise role of SOCE in skeletal muscle contractility is not clear. The dependence on SOCE during cardiac and smooth muscle contractility is even less certain. Here, we will hypothesize on the contribution of SOCE in muscle and its potential role in contractility and signaling.
Authors:
Mohamed Trebak; Wei Zhang; Brian Ruhle; Matthew M Henkel; José C González-Cobos; Rajender K Motiani; Judith A Stolwijk; Rachel L Newton; Xuexin Zhang
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Microcirculation (New York, N.Y. : 1994)     Volume:  20     ISSN:  1549-8719     ISO Abbreviation:  Microcirculation     Publication Date:  2013 May 
Date Detail:
Created Date:  2013-05-10     Completed Date:  2013-12-09     Revised Date:  2014-05-07    
Medline Journal Info:
Nlm Unique ID:  9434935     Medline TA:  Microcirculation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  330-6     Citation Subset:  IM    
Copyright Information:
© 2013 John Wiley & Sons Ltd.
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MeSH Terms
Descriptor/Qualifier:
Animals
Calcium / metabolism*
Calcium Channels / metabolism*
Calcium Signaling / physiology*
Cell Membrane / metabolism
Humans
Membrane Proteins / metabolism*
Muscle, Skeletal / metabolism*
Muscle, Smooth / metabolism*
Neoplasm Proteins / metabolism*
Grant Support
ID/Acronym/Agency:
HL097111/HL/NHLBI NIH HHS; R01 HL097111/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Calcium Channels; 0/Membrane Proteins; 0/Neoplasm Proteins; 0/ORAI1 protein, human; 0/STIM1 protein, human; SY7Q814VUP/Calcium
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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