By H. R. Colten (auth.), Prof. Dr. Martha M. Eibl, Prof. Dr. Christoph Huber, Prof. Dr. Hans H. Peter, Prof. Dr. Ulrich Wahn (eds.)
This booklet, the final in a chain of 8 complaints volumes, offers an updated evaluation on immunology and irritation in accordance with a congress held in Budapest, Hungary in April 1998. it truly is divided into the subsequent sections: easy Mechanisms, Endo- and Exotoxins, Soluble Receptors, and remedy Perspectives.
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Extra info for Symposium in Immunology VIII: Inflammation
In most cell types, NF-1
First, in a simple mechanistic model, sPLAz-triggered inflammatory reaction comprises the generation of arachidonic acid and lysophospholipids, which are subsequently metabolized into eicosanoids and platelet-activating factor. Moreover, arachidonic acid and lysophospholipids may themselves act as signaling molecules. An especially intriguing possibility is a sPLAz-induced activation of PKC. Both products of PLAz's catalytic action, lysophosphatidylcholine (LPC) and cis-unsaturated fatty acids, including arachidonic acid, have previously been shown to amplify hormone-induced cellular responses by enhancing the 1,2-diacylglycerol-stimulated activation of PKC.
1997). However, differences exist between both kinases in their relative activities. IKK-~ is constitutively active when transfected alone, whereas the activity of IKK-u is relatively low and requires costimulation by TNF to become fully active. , 1997). ,1997). , 1997). , 1997). , 1997). , 1997). , 1997). , 1997). ,1997). , 1997). , 1998). Both IKK-u and IKK-~ contain canonical MAP kinase kinase (MAPKK) activation loops in their catalytic domains (Ser-X-X-X-Ser, where X can be any amino acid) which represent putative phosphorylation sites for Activation of NF-KB by Inflammatory Cytokines 37 upstream MAPKKKs such as NIK or MEKK1 (for review see May and Gosh, 1998).