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rdf:type |
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lifeskim:mentions |
umls-concept:C0007600,
umls-concept:C0024432,
umls-concept:C0040649,
umls-concept:C0042071,
umls-concept:C0079784,
umls-concept:C0441889,
umls-concept:C0591833,
umls-concept:C0597357,
umls-concept:C0851285,
umls-concept:C0851827,
umls-concept:C1522670,
umls-concept:C1701901
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pubmed:dateCreated |
2000-6-5
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pubmed:abstractText |
Macrophage colony-stimulating factor (CSF-1) binds to a receptor (CSF-1R) encoded by the c-fms proto-oncogene and activates transcription of the urokinase plasminogen activator (uPA) gene in murine bone-marrow-derived macrophages. This article demonstrates that the murine macrophage cell line RAW264 responds to CSF-1 with inducible phosphorylation of cytoplasmic proteins on tyrosine residues but fails to induce transcription of uPA. The defect was correlated with a selective failure to maintain CSF-1Rs on the cell surface, whereas all RAW264 cells contained abundant CSF-1Rs within the presumptive Golgi/endoplasmic reticulum compartment. Transfection with a CSF-1R expression plasmid permitted CSF-1-dependent activation of the signalling pathway targeting an Ets/AP1 (activator protein 1) element in the uPA promoter that has been shown previously to be a target of oncogenic ras and protein kinase C pathways. Mutation of the expressed CSF-1R at either Y807 or Y559, sites of receptor tyrosine phosphorylation implicated in signal transduction, reduced but did not abolish uPA promoter activation by CSF-1. Activation by mutant CSF-1R plasmids was additive; there was no evidence of mutual complementation. The results indicate that maintenance of elevated uPA transcription by CSF-1 requires new receptors emerging continuously on the cell surface. Parallel, partly redundant, signalling pathways arising from phosphorylated tyrosines on the CSF-1R activate multiple cis-acting elements on the complex uPA promoter.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-1698283,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-1833648,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-212198,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-3518947,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-6607172,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-7478559,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-7520523,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-7528686,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-7545432,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-7579387,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-7681396,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-7730365,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-7760840,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-7782294,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-7834738,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-7953555,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-8217790,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-8253768,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-8486399,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-8545103,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-8550554,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-8552081,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-8570190,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-8654924,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-8668185,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-9261328,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-9312046,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-9409785,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-9642280,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-9710599,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-9804836,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-9824165,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10727433-9857184
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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 |
Apr
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pubmed:issn |
0264-6021
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
347 Pt 1
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
313-20
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:10727433-Amino Acid Substitution,
pubmed-meshheading:10727433-Animals,
pubmed-meshheading:10727433-Cell Line,
pubmed-meshheading:10727433-Gene Expression Regulation, Enzymologic,
pubmed-meshheading:10727433-Macrophage Colony-Stimulating Factor,
pubmed-meshheading:10727433-Macrophages,
pubmed-meshheading:10727433-Mice,
pubmed-meshheading:10727433-Mutagenesis, Site-Directed,
pubmed-meshheading:10727433-Phosphorylation,
pubmed-meshheading:10727433-Phosphotyrosine,
pubmed-meshheading:10727433-Promoter Regions, Genetic,
pubmed-meshheading:10727433-Receptor, Macrophage Colony-Stimulating Factor,
pubmed-meshheading:10727433-Recombinant Proteins,
pubmed-meshheading:10727433-Signal Transduction,
pubmed-meshheading:10727433-Transcription, Genetic,
pubmed-meshheading:10727433-Transfection,
pubmed-meshheading:10727433-Urokinase-Type Plasminogen Activator
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pubmed:year |
2000
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pubmed:articleTitle |
Regulation of urokinase plasminogen activator gene transcription in the RAW264 murine macrophage cell line by macrophage colony-stimulating factor (CSF-1) is dependent upon the level of cell-surface receptor.
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pubmed:affiliation |
Department of Biochemistry, Centre for Molecular and Cellular Biology, The University of Queensland, Q4072, Australia.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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