Research Topics
Species | M U MartinSummaryAffiliation: Hannover Medical School Country: Germany Publications
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Detail Information
Publications
Summary and comparison of the signaling mechanisms of the Toll/interleukin-1 receptor familyMichael U Martin
Institute of Pharmacology OE 5320, Hannover Medical School, Germany
Biochim Biophys Acta 1592:265-80. 2002..The creation of pathogen-specific mediator environments by dendritic cells defines whether a cellular or humoral response will be activated in response to the pathogen...
The interleukin 1 (IL-1) receptor accessory protein Toll/IL-1 receptor domain: analysis of putative interaction sites in vitro mutagenesis and molecular modelingJurgen Radons
Klinik und Poliklinik für Innere Medizin I, Universitat Regensburg, D 93042 Regensburg, Germany
J Biol Chem 278:49145-53. 2003....
The interleukin-1 receptor complex and interleukin-1 signal transductionM U Martin
Medical School Hannover, Germany
Eur Cytokine Netw 8:5-17. 1997..It is not the aim of this review to extensively summarize IL-1 induced cytosolic kinase cascades and activation of transcription factors...
The interleukin-1 receptor accessory protein (IL-1RAcP) is essential for IL-1-induced activation of interleukin-1 receptor-associated kinase (IRAK) and stress-activated protein kinases (SAP kinases)H Wesche
Department of Molecular Pharmacology, Medical School Hannover, D 30623 Hannover, Germany
J Biol Chem 272:7727-31. 1997....
Interleukin-12 upregulates the IL-18Rbeta chain in BALB/c thymocytesD Neumann
Pharmacology OE 5320, Hannover Medical School, D-30623 Hannover, Germany
J Interferon Cytokine Res 21:635-42. 2001..Thus, the synergistic effects of IL-12 and IL-18 on BALB/c mouse thymocytes resulted from the induction and regulation of the IL-18Rbeta chain and not the IL-18Ralpha chain...
Stimulation of toll-like receptor 4 expression in human mononuclear phagocytes by interferon-gamma: a molecular basis for priming and synergism with bacterial lipopolysaccharideDaniela Bosisio
Department of Immunology and Cell Biology, Mario Negri Institute, Milano, Italy
Blood 99:3427-31. 2002..These results suggest that enhanced TLR4 expression underlies the long-known priming by IFNgamma of mononuclear phagocytes for pathogen recognition and killing as well as its synergism with LPS in macrophage activation...
Identification and characterization of murine IRAK-MOlaf Rosati
Institute of Pharmacology, Hannover Medical School, D 30623 Hannover, Germany
Biochem Biophys Res Commun 293:1472-7. 2002....
Identification and characterization of murine IRAK-2Olaf Rosati
Institute of Pharmacology, Hannover Medical School, D 30623 Hannover, Germany
Biochem Biophys Res Commun 297:52-8. 2002....
IL-1beta-induced phosphorylation of PKB/Akt depends on the presence of IRAK-1Detlef Neumann
Hannover Medical School, Department of Pharmacology, Hannover, Germany
Eur J Immunol 32:3689-98. 2002..Possible models of the interaction between IRAK-1 and the PI3-K pathway are discussed...
Sequential autophosphorylation steps in the interleukin-1 receptor-associated kinase-1 regulate its availability as an adapter in interleukin-1 signalingChristian Kollewe
Department of Pharmacology, Hannover Medical School, D 30623 Hannover, Germany
J Biol Chem 279:5227-36. 2004..Thus, IRAK-1 regulates its own availability as an adapter molecule by sequential autophosphorylation...
The death domain of IRAK-1: an oligomerization domain mediating interactions with MyD88, Tollip, IRAK-1, and IRAK-4Detlef Neumann
Department for Pharmacology, Hannover Medical School, Carl Neuberg Str 1, D 30623 Hannover, Germany
Biochem Biophys Res Commun 354:1089-94. 2007..Finally, mutation of IRAK-1 at T66 not only allowed stable binding to the signaling adapters, but also enhanced its signaling capacity...
Threonine 66 in the death domain of IRAK-1 is critical for interaction with signaling molecules but is not a target site for autophosphorylationDetlef Neumann
Deptartment of Pharmacology, Hannover Medical School, Hannover, Germany
J Leukoc Biol 84:807-13. 2008..Thereby, it ensures the transient manner of interactions between IRAK-1 and the other signaling molecules. This essential role, however, is not regulated by phosphorylation of T66 itself...
