| pubmed-article:16164016 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16164016 | lifeskim:mentions | umls-concept:C0079784 | lld:lifeskim |
| pubmed-article:16164016 | lifeskim:mentions | umls-concept:C2697656 | lld:lifeskim |
| pubmed-article:16164016 | lifeskim:mentions | umls-concept:C0175697 | lld:lifeskim |
| pubmed-article:16164016 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
| pubmed-article:16164016 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
| pubmed-article:16164016 | lifeskim:mentions | umls-concept:C0023810 | lld:lifeskim |
| pubmed-article:16164016 | lifeskim:mentions | umls-concept:C0441472 | lld:lifeskim |
| pubmed-article:16164016 | lifeskim:mentions | umls-concept:C0036849 | lld:lifeskim |
| pubmed-article:16164016 | lifeskim:mentions | umls-concept:C1442518 | lld:lifeskim |
| pubmed-article:16164016 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:16164016 | lifeskim:mentions | umls-concept:C1552652 | lld:lifeskim |
| pubmed-article:16164016 | lifeskim:mentions | umls-concept:C0205225 | lld:lifeskim |
| pubmed-article:16164016 | lifeskim:mentions | umls-concept:C1552685 | lld:lifeskim |
| pubmed-article:16164016 | lifeskim:mentions | umls-concept:C1705195 | lld:lifeskim |
| pubmed-article:16164016 | lifeskim:mentions | umls-concept:C0591833 | lld:lifeskim |
| pubmed-article:16164016 | pubmed:issue | 2-4 | lld:pubmed |
| pubmed-article:16164016 | pubmed:dateCreated | 2005-9-16 | lld:pubmed |
| pubmed-article:16164016 | pubmed:abstractText | We previously reported that bacterial products such as LPS and CpG DNA down-modulated cell surface levels of the Colony Stimulating Factor (CSF)-1 receptor (CSF-1R) on primary murine macrophages in an all-or-nothing manner. Here we show that the ability of bacterial products to down-modulate the CSF-1R rendered bone marrow-derived macrophages (BMM) unresponsive to CSF-1 as assessed by Akt and ERK1/2 phosphorylation. Using toll-like receptor (tlr)9 as a model CSF-1-repressed gene, we show that LPS induced tlr9 expression in BMM only when CSF-1 was present, suggesting that LPS relieves CSF-1-mediated inhibition to induce gene expression. Using cDNA microarrays, we identified a cluster of similarly CSF-1 repressed genes in BMM. By real time PCR we confirmed that the expression of a selection of these genes, including integral membrane protein 2B (itm2b), receptor activity-modifying protein 2 (ramp2) and macrophage-specific gene 1 (mpg-1), were repressed by CSF-1 and were induced by LPS only in the presence of CSF-1. This pattern of gene regulation was also apparent in thioglycollate-elicited peritoneal macrophages (TEPM). LPS also counteracted CSF-1 action to induce mRNA expression of a number of transcription factors including interferon consensus sequence binding protein 1 (Icsbp1), suggesting that this mechanism leads to transcriptional reprogramming in macrophages. Since the majority of in vitro studies on macrophage biology do not include CSF-1, these genes represent a set of previously uncharacterised LPS-inducible genes. This study identifies a new mechanism of macrophage activation, in which LPS (and other toll-like receptor agonists) regulate gene expression by switching off the CSF-1R signal. This finding also provides a biological relevance to the well-documented ability of macrophage activators to down-modulate surface expression of the CSF-1R. | lld:pubmed |
| pubmed-article:16164016 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16164016 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16164016 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16164016 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16164016 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16164016 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16164016 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16164016 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16164016 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16164016 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16164016 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16164016 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16164016 | pubmed:issn | 0171-2985 | lld:pubmed |
| pubmed-article:16164016 | pubmed:author | pubmed-author:RavasiTimothy... | lld:pubmed |
| pubmed-article:16164016 | pubmed:author | pubmed-author:HumeDavid ADA | lld:pubmed |
| pubmed-article:16164016 | pubmed:author | pubmed-author:SweetMatthew... | lld:pubmed |
| pubmed-article:16164016 | pubmed:author | pubmed-author:SesterDavid... | lld:pubmed |
| pubmed-article:16164016 | pubmed:author | pubmed-author:McDonaldRebec... | lld:pubmed |
| pubmed-article:16164016 | pubmed:author | pubmed-author:StaceyKatryn... | lld:pubmed |
| pubmed-article:16164016 | pubmed:author | pubmed-author:HayashizakiYo... | lld:pubmed |
| pubmed-article:16164016 | pubmed:author | pubmed-author:SuzukiHarukaz... | lld:pubmed |
| pubmed-article:16164016 | pubmed:author | pubmed-author:RobinsonJodie... | lld:pubmed |
| pubmed-article:16164016 | pubmed:author | pubmed-author:WellsChristin... | lld:pubmed |
| pubmed-article:16164016 | pubmed:author | pubmed-author:SchroderKateK | lld:pubmed |
| pubmed-article:16164016 | pubmed:author | pubmed-author:TrieuAngelaA | lld:pubmed |
| pubmed-article:16164016 | pubmed:author | pubmed-author:BrionKristian... | lld:pubmed |
| pubmed-article:16164016 | pubmed:author | pubmed-author:RipollVeraV | lld:pubmed |
| pubmed-article:16164016 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16164016 | pubmed:volume | 210 | lld:pubmed |
| pubmed-article:16164016 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16164016 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16164016 | pubmed:pagination | 97-107 | lld:pubmed |
| pubmed-article:16164016 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
| pubmed-article:16164016 | pubmed:meshHeading | pubmed-meshheading:16164016... | lld:pubmed |
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| pubmed-article:16164016 | pubmed:meshHeading | pubmed-meshheading:16164016... | lld:pubmed |
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| pubmed-article:16164016 | pubmed:meshHeading | pubmed-meshheading:16164016... | lld:pubmed |
| pubmed-article:16164016 | pubmed:meshHeading | pubmed-meshheading:16164016... | lld:pubmed |
| pubmed-article:16164016 | pubmed:meshHeading | pubmed-meshheading:16164016... | lld:pubmed |
| pubmed-article:16164016 | pubmed:meshHeading | pubmed-meshheading:16164016... | lld:pubmed |
| pubmed-article:16164016 | pubmed:meshHeading | pubmed-meshheading:16164016... | lld:pubmed |
| pubmed-article:16164016 | pubmed:meshHeading | pubmed-meshheading:16164016... | lld:pubmed |
| pubmed-article:16164016 | pubmed:meshHeading | pubmed-meshheading:16164016... | lld:pubmed |
| pubmed-article:16164016 | pubmed:meshHeading | pubmed-meshheading:16164016... | lld:pubmed |
| pubmed-article:16164016 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:16164016 | pubmed:articleTitle | LPS regulates a set of genes in primary murine macrophages by antagonising CSF-1 action. | lld:pubmed |
| pubmed-article:16164016 | pubmed:affiliation | Cooperative Research Centre for Chronic Inflammatory Diseases, Institute for Molecular Bioscience, University of Queensland, Brisbane, Queensland 4072, Australia. | lld:pubmed |
| pubmed-article:16164016 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16164016 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16164016 | lld:pubmed |
