For the JAK-STAT, MAP kinase, and NF- κB pathways a lot of biological insight is available, and as a consequence, large mathematical models have emerged.
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A critical signalling pathway involved in mediating an inflammatory response is the JAK-STAT and MAP kinase pathway.
The method, which we refer to as the eigenvalue method, was applied to existing models of the JAK-STAT, the MAP kinase, and the NF- κB pathways.
The interaction of the selective, nonpeptidyl TPO-R agonist, eltrombopag, with TPO-R triggers activation of the JAK-STAT and MAP kinase, but not the AKT, signal transduction pathways.
In fact the eigenvalue method stops after three, two, and three iterations in the JAK-STAT, the MAP kinase, and the NF- κB case, respectively, and therefore turns out to be far less computationally expensive than under the worst case assumption used in Appendix E. From a technical point of view, the correlation method suffers from two drawbacks.
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We identify one dimeric TM conformation that imparts full activity to the cytosolic domain of the receptor and signals via JAK2, STAT proteins, and MAP kinase, one partially active orientation that preferentially activates MAP kinase, and one conformation corresponding to the inactive receptor.
A putative GAS element that could provide a STAT binding site mapped to this region, and its mutation decreased PRL-responsiveness.
