Historical Background
The IGF1R, a Protein Tyrosine Kinase Receptor, is expressed in many tissues and can be activated by its physiological ligands IGF-I and IGF-II, which are available systemically and from local sources. Activation of the IGF1R promotes cell growth and survival in a cell-autonomous manner. Because of a wide distribution of IGF1R and good bioavailability of its ligands, under pathological conditions this cytoprotective intracellular signaling pathway may be activated in cells that also receive stimulation by pathology-specific factors. Cross-regulation between IGF1R signaling and pathways activated by inflammation has recently been in the focus of attention in several laboratories because pro-inflammatory factors are a common cause of cellular pathology in many different conditions (O’Connor et al. 2008).
Resident parenchymal cells activated by pro-inflammatory cytokines in tissues affected by inflammation...
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Annenkov, A. (2018). Insulin-Like Growth Factor Receptor Type I (IGF1R) Signaling and Inflammation. In: Choi, S. (eds) Encyclopedia of Signaling Molecules. Springer, Cham. https://doi.org/10.1007/978-3-319-67199-4_326
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