Source:http://linkedlifedata.com/resource/pubmed/id/10682899
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2000-3-1
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pubmed:abstractText |
Neurotransmitter-regulation of fluid secretion in the salivary glands is achieved by a coordinated sequence of intracellular signaling events, including the activation of membrane receptors, generation of the intracellular second messenger, inositol 1,4,5, trisphosphate, internal Ca2+ release, and Ca2+ influx. The resulting increase in cytosolic [Ca2+] ([Ca2+]i) regulates a number of ion transporters, e.g., Ca2+-activated K+ channel, Na+/K+/2Cl- co-transporter in the basolateral membrane, and the Ca2+-activated Cl- channel in the luminal membrane, which are intricately involved in fluid secretion. Thus, regulation of [Ca2+]i is central to the regulation of salivary acinar cell function and is achieved by the concerted activities of several ion channels and Ca2+-pumps localized in various cellular membranes. Ca2+ pumps, present in the endoplasmic reticulum and the plasma membrane, serve to remove Ca2+ from the cytosol. Ca2+ channels present in the endoplasmic reticulum and the plasma membrane facilitate rapid influx of Ca2+ into the cytosol from the internal Ca2+ stores and from the external medium, respectively. It is well-established that prolonged fluid secretion is regulated via a sustained elevation in [Ca2+]i that is primarily achieved by the influx of Ca2+ into the cell from the external medium. This Ca2+ influx occurs via a putative plasma-membrane-store-operated Ca2+ channel which has not yet been identified in any non-excitable cell type. Understanding the molecular nature of this Ca2+ influx mechanism is critical to our understanding of Ca2+ signaling in salivary gland cells. This review focuses on the various active and passive Ca2+ transport mechanisms in salivary gland cells--their localization, regulation, and role in neurotransmitter-regulation of fluid secretion. In addition to a historical perspective of Ca2+ signaling, recent findings and challenging problems facing this field are highlighted.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
D
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
1045-4411
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
11
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4-25
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:10682899-Animals,
pubmed-meshheading:10682899-Calcium,
pubmed-meshheading:10682899-Calcium Channels,
pubmed-meshheading:10682899-Calcium Signaling,
pubmed-meshheading:10682899-Calcium-Binding Proteins,
pubmed-meshheading:10682899-Calcium-Transporting ATPases,
pubmed-meshheading:10682899-Cell Membrane,
pubmed-meshheading:10682899-Humans,
pubmed-meshheading:10682899-Salivary Glands,
pubmed-meshheading:10682899-Salivation
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pubmed:year |
2000
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pubmed:articleTitle |
Regulation of calcium in salivary gland secretion.
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pubmed:affiliation |
Secretory Physiology Section, Gene Therapy and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland 20892, USA.
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pubmed:publicationType |
Journal Article,
Review
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