Download Symposium in Immunology VIII: Inflammation by H. R. Colten (auth.), Prof. Dr. Martha M. Eibl, Prof. Dr. PDF

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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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).

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