Linked Life Data

20392259

Source:http://linkedlifedata.com/resource/pubmed/id/20392259

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2010-4-15
pubmed:abstractText
Calcium plays multiple roles in osteoclast formation, survival, and activity. Intracellular calcium is determined both by the release of intracellular stores and the influx of extracellular calcium through a variety of calcium channels. Osteoclasts express several classes of calcium channels, including ryanodine receptors (RyRs), inositol-1,4,5-trisphosphate receptors (IP(3)Rs), and calcium release-activated calcium channels (CRACs), which respond to depletion of intracellular stores. IP(3)R2 is expressed in osteoclast precursors and activated by cytokines that stimulate osteoclast differentiation. In mature osteoclasts, the IP(3)R1 isoform is highly expressed and is implicated in nitric oxide-cGMP-stimulated processes. RyR calcium channels may contribute to the release of intracellular calcium stores, while RyR2 in the plasma membrane may act to limit osteoclast activity based on extracellular calcium concentration. Orai, through regulation by endoplasmic reticular store-sensing proteins, including Stim-1, may also mediate calcium influx and act as a signal amplifier for calcium release by other calcium channels. Together, these receptors allow intracellular Ca(2+) signals to modulate bone turnover and, through calcium-sensing functions, allow coupling of osteoclast activity to extracellular conditions and integrating additional cytokine and nitric oxide signals via transient intracellular calcium signals.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1749-6632
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
1192
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
351-7
pubmed:dateRevised
2010-10-19
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Regulation of bone turnover by calcium-regulated calcium channels.
pubmed:affiliation
Department of Pathology, University of Pittsburgh, Pittsburgh, PA, USA. robinsonlj@upmc.edu
pubmed:publicationType
Journal Article, Review