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rdf:type |
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lifeskim:mentions |
umls-concept:C0021755,
umls-concept:C0030685,
umls-concept:C0109317,
umls-concept:C0205102,
umls-concept:C0205263,
umls-concept:C0391871,
umls-concept:C0596235,
umls-concept:C0680255,
umls-concept:C0752312,
umls-concept:C0851285,
umls-concept:C0851827,
umls-concept:C1150579,
umls-concept:C1283071,
umls-concept:C1333340,
umls-concept:C1366882,
umls-concept:C1370600,
umls-concept:C1698986,
umls-concept:C1701901,
umls-concept:C1704675,
umls-concept:C1705767,
umls-concept:C1705791,
umls-concept:C1879547,
umls-concept:C1963578
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pubmed:issue |
13
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pubmed:dateCreated |
2003-10-1
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pubmed:abstractText |
The cellular mechanisms that modulate interleukin-1 (IL-1) signaling are not defined. In fibroblasts, IL-1 signaling is affected by the nature of cell-matrix adhesions including focal adhesions, adhesive domains that sequester IL-1 receptors. We conducted studies to elucidate which steps of cellular Ca2+ handling are affected by focal adhesions and by which mechanisms focal adhesions modulate IL-1-induced Ca2+ signals and ERK activation in human gingival fibroblasts. Cells were plated on poly-l-lysine or fibronectin and treated with tenascin, Hep-I, or SPARC peptides to inhibit focal adhesion formation. These treatments blocked IL-1 and thapsigargin-induced Ca2+ release from the endoplasmic reticulum, indicating that the ER-release pathway is focal adhesion dependent. Focal adhesions were also required for Ca2+ entry through store-operated channels and for IL-1-induced ERK activation. Thus interactions with the extracellular matrix and focal adhesion formation regulate IL-1-induced generation of intracellular Ca2+ signals that in turn are required for ERK activation.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1530-6860
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
17
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1898-900
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:14519666-Calcium,
pubmed-meshheading:14519666-Calcium Channels,
pubmed-meshheading:14519666-Calcium Signaling,
pubmed-meshheading:14519666-Cell Adhesion,
pubmed-meshheading:14519666-Enzyme Activation,
pubmed-meshheading:14519666-Fibroblasts,
pubmed-meshheading:14519666-Focal Adhesions,
pubmed-meshheading:14519666-Humans,
pubmed-meshheading:14519666-Interleukin-1,
pubmed-meshheading:14519666-Mitogen-Activated Protein Kinases,
pubmed-meshheading:14519666-Models, Biological,
pubmed-meshheading:14519666-Oligopeptides,
pubmed-meshheading:14519666-Osteonectin,
pubmed-meshheading:14519666-Phosphorylation,
pubmed-meshheading:14519666-Tenascin
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pubmed:year |
2003
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pubmed:articleTitle |
IL-1 induced release of Ca2+ from internal stores is dependent on cell-matrix interactions and regulates ERK activation.
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pubmed:affiliation |
CIHR Group in Matrix Dynamics, University of Toronto, Toronto, Ontario M5S 3E2, Canada.
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pubmed:publicationType |
Journal Article
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