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- aggregation classification "A1".
- aggregation creator B449186.
- aggregation creator B449187.
- aggregation creator B449188.
- aggregation creator B449189.
- aggregation creator B449190.
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- aggregation creator B449194.
- aggregation creator person.
- aggregation date "2009".
- aggregation format "application/pdf".
- aggregation hasFormat 818088.bibtex.
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- aggregation isPartOf urn:issn:0282-0080.
- aggregation language "eng".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Biology and Life Sciences".
- aggregation title "Dependence of pathogen molecule-induced Toll-like receptor activation and cell function on Neu1 sialidase".
- aggregation abstract "The signaling pathways of mammalian Toll-like receptors (TLR) are well characterized, but the initial molecular mechanisms activated following ligand interactions with the receptors remain poorly defined. Here, we show a membrane controlling mechanism that is initiated by ligand binding to TLR-2, -3 and-4 to induce Neu1 sialidase activity within minutes in live primary bone marrow (BM) macrophage cells and macrophage and dendritic cell lines. Central to this process is that Neu1 and not Neu2,-3 and-4 forms a complex with TLR-2,-3 and-4 on the cell surface of na < ve macrophage cells. Neuraminidase inhibitors BCX1827, 2-deoxy-2,3-dehydro-N-acetylneuraminic acid (DANA), zanamivir and oseltamivir carboxylate have a limited significant inhibition of the LPS-induced sialidase activity in live BMC-2 macrophage cells but Tamiflu (oseltamivir phosphate) completely blocks this activity. Tamiflu inhibits LPS-induced sialidase activity in live BMC-2 cells with an IC50 of 1.2 mu M compared to an IC50 of 1015 mu M for its hydrolytic metabolite oseltamivir carboxylate. Tamiflu blockage of LPS-induced Neu1 sialidase activity is not affected in BMC-2 cells pretreated with anticarboxylesterase agent clopidogrel. Endotoxin LPS binding to TLR4 induces Neu1 with subsequent activation of NF kappa B and the production of nitric oxide and pro-inflammatory IL-6 and TNF alpha cytokines in primary and macrophage cell lines. Hypomorphic cathepsin A mice with a secondary Neu1 deficiency respond poorly to LPS-induced pro-inflammatory cytokines compared to the wild-type or hypomorphic cathepsin A with normal Neu1 mice. Our findings establish an unprecedented mechanism for pathogen molecule-induced TLR activation and cell function, which is critically dependent on Neu1 sialidase activity associated with TLR ligand treated live primary macrophage cells and macrophage and dendritic cell lines.".
- aggregation authorList BK783404.
- aggregation endPage "1212".
- aggregation issue "9".
- aggregation startPage "1197".
- aggregation volume "26".
- aggregation aggregates 2937062.
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- aggregation similarTo s10719-009-9239-8.
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