Cutting Edge: Preferentially the R-Stereoisomer of the Mycoplasmal Lipopeptide Macrophage-Activating Lipopeptide-2 Activates Immune Cells Through a Toll-Like Receptor 2- and MyD88-Dependent…
By O. Takeuchi, A. Kaufmann, K. Grote, Taro Kawai, K. Hoshino, M. Morr, P. Mühlradt, Shizuo Akira. Journal of Immunology, 2000
641 citations recorded by the source corpus.
Subfields: Immunology, Microbiology
View Paper: https://www.semanticscholar.org/paper/8d7fbb72a3b357b647d90fd781ac18e0b1713ca1
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In Immunology
In Microbiology
Citations in the corpus
- Cutting Edge: Repurification of Lipopolysaccharide Eliminates Signaling Through Both Human and Murine Toll-Like Receptor 21 (2000, background): “Although we have not characterized the biochemical nature of the contaminants responsible for TLR2-mediated signaling, it seems likely that bacterial lipoproteins could be at least partially responsible, given past reports demonstrating lipoprotein signaling mediated by TLR2 (18, 20, 22, 23, 26).”
- Cutting Edge: A Novel Toll/IL-1 Receptor Domain-Containing Adapter That Preferentially Activates the IFN-β Promoter in the Toll-Like Receptor Signaling1 (2002, neutral): “Macrophageactivating lipopeptide (2 kDa; MALP-2) and R-848 were described previously (11, 12).”
- Toll-like receptors. (2003, background): “Analysis of TLR2deficient mice showed that TLR2 is critical to the recognition of peptidoglycan and lipoproteins (99, 100).”
- TLR signaling pathways. (2004, background): “The cellular responses to the TLR2 ligands peptidoglycan and lipoproteins were abolished in MyD88 knockout mice [10,11].”