| pubmed-article:16848641 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16848641 | lifeskim:mentions | umls-concept:C0021311 | lld:lifeskim |
| pubmed-article:16848641 | lifeskim:mentions | umls-concept:C0036971 | lld:lifeskim |
| pubmed-article:16848641 | lifeskim:mentions | umls-concept:C0317549 | lld:lifeskim |
| pubmed-article:16848641 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
| pubmed-article:16848641 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
| pubmed-article:16848641 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
| pubmed-article:16848641 | lifeskim:mentions | umls-concept:C1416447 | lld:lifeskim |
| pubmed-article:16848641 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
| pubmed-article:16848641 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
| pubmed-article:16848641 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:16848641 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:16848641 | pubmed:dateCreated | 2006-7-19 | lld:pubmed |
| pubmed-article:16848641 | pubmed:abstractText | Francisella tularensis, a Gram-negative facultative intracellular pathogen infecting principally macrophages and monocytes, is the etiological agent of tularemia. Macrophage responses to F. tularensis infection include the production of pro-inflammatory cytokines such as interleukin (IL)-12, which is critical for immunity against infection. Molecular mechanisms regulating production of these inflammatory mediators are poorly understood. Herein we report that the SH2 domain-containing inositol phosphatase (SHIP) is phosphorylated upon infection of primary murine macrophages with the genetically related F. novicida, and negatively regulates F. novicida-induced cytokine production. Analyses of the molecular details revealed that in addition to activating the MAP kinases, F. novicida infection also activated the phosphatidylinositol 3-kinase (PI3K)/Akt pathway in these cells. Interestingly, SHIP-deficient macrophages displayed enhanced Akt activation upon F. novicida infection, suggesting elevated PI3K-dependent activation pathways in absence of SHIP. Inhibition of PI3K/Akt resulted in suppression of F. novicida-induced cytokine production through the inhibition of NFkappaB. Consistently, macrophages lacking SHIP displayed enhanced NFkappaB-driven gene transcription, whereas overexpression of SHIP led to decreased NFkappaB activation. Thus, we propose that SHIP negatively regulates F. novicida-induced inflammatory cytokine response by antagonizing the PI3K/Akt pathway and suppressing NFkappaB-mediated gene transcription. A detailed analysis of phosphoinositide signaling may provide valuable clues for better understanding the pathogenesis of tularemia. | lld:pubmed |
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| pubmed-article:16848641 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16848641 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16848641 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16848641 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16848641 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:16848641 | pubmed:issn | 1553-7374 | lld:pubmed |
| pubmed-article:16848641 | pubmed:author | pubmed-author:WewersMark... | lld:pubmed |
| pubmed-article:16848641 | pubmed:author | pubmed-author:TridandapaniS... | lld:pubmed |
| pubmed-article:16848641 | pubmed:author | pubmed-author:SchlesingerLa... | lld:pubmed |
| pubmed-article:16848641 | pubmed:author | pubmed-author:GunnJohn SJS | lld:pubmed |
| pubmed-article:16848641 | pubmed:author | pubmed-author:GavrilinMikha... | lld:pubmed |
| pubmed-article:16848641 | pubmed:author | pubmed-author:GanesanLatha... | lld:pubmed |
| pubmed-article:16848641 | pubmed:author | pubmed-author:ParsaKishore... | lld:pubmed |
| pubmed-article:16848641 | pubmed:author | pubmed-author:BalagopalAshw... | lld:pubmed |
| pubmed-article:16848641 | pubmed:author | pubmed-author:RajaramMuruge... | lld:pubmed |
| pubmed-article:16848641 | pubmed:author | pubmed-author:MohapatraNrus... | lld:pubmed |
| pubmed-article:16848641 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:16848641 | pubmed:volume | 2 | lld:pubmed |
| pubmed-article:16848641 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16848641 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16848641 | pubmed:pagination | e71 | lld:pubmed |
| pubmed-article:16848641 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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