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EGF–ERBB signalling: towards the systems level
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Journal Article
EGF–ERBB signalling: towards the systems level
2006
Overview
Key Points
The ERBB system consists of four receptors (ERBB1–4), two of which, ERBB2/HER2 and ERBB3 are non-autonomous. All four ERBB proteins form functional dimers after activation by epidermal growth factor (EGF)-family growth factors.
Recent advances in structural analysis of the receptors has revealed the mechanism of receptor dimerization, and together with the results of gene targeting in mice provide an explanation for the critical role of ERBB2/HER2 in human cancer.
Misregulated activation of ERBB receptors has been widely associated with human malignancies, and a number of drugs that target these receptors are in clinical use.
∼25,000 scientific papers relate to ERBB-receptor signalling, in which hundreds of receptor interactions are described, forcing investigators to take a systems view of the network.
Definitions from the field of systems biology apply to the ERBB network, which is described as a robust information-processing system, with a bow-tie structure, to which we apply principles of modularity, redundancy, bistability, system controls and buffering.
Fragility of the system is a necessary trade-off of its robustness, a principle we exemplify when dealing with clinically approved, as well as experimental, cancer therapeutics.
Future analysis of the ERBB network might depend on establishing common experimental conditions, which will allow synergistic interactions between experimentalists and theoreticians in the field.
The ERBB network is one of the most studied areas in signal transduction, and it exemplifies the pathogenic power of aberrant signalling. Systems-level modelling and an understanding of the network's circuitry, robustness and controls will enable the development of novel cancer therapies.
Signalling through the ERBB/HER receptors is intricately involved in human cancer and already serves as a target for several cancer drugs. Because of its inherent complexity, it is useful to envision ERBB signalling as a bow-tie-configured, evolvable network, which shares modularity, redundancy and control circuits with robust biological and engineered systems. Because network fragility is an inevitable trade-off of robustness, systems-level understanding is expected to generate therapeutic opportunities to intercept aberrant network activation.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Biology
/ Biomedical and Life Sciences
/ Epidermal Growth Factor - metabolism
/ Humans
/ Kinases
/ Ligands
/ Oncogene Proteins v-erbB - genetics
/ Oncogene Proteins v-erbB - metabolism
/ Phosphatidylinositol 3-Kinases - metabolism
/ Proteins
/ Receptor, Epidermal Growth Factor - chemistry
/ Receptor, Epidermal Growth Factor - genetics
/ Receptor, Epidermal Growth Factor - metabolism
