Signal transduction: specificity of growth factors explained by parallel distributed processing.
Mutations in proteins of receptor tyrosine kinase signalling pathways might change signalling properties and contribute to the progression towards neoplasia. Ligands for these receptors (growth factors) which elicit the same signal transducing cascades can trigger different developmental pathways in identical cells. For example, PC12 cells differentiate after treatment with NGF, but proliferate after stimulation with EGF. However, their receptors seem to utilize the same signal transducing components. Thus, intracellular signalling specificity remains an enigma. Here, we apply a network model, in which each protein species participating in signal transduction is represented by an element. The elements are connected to each other according to the signalling pathways resembling parallel distributed processes. A general property of these systems is applied to the problem of signal specificity: slight differences in the input may result in completely different outputs, which negates the necessity of specific proteins to each pathway. This line of thinking might explain the specificity of hormones, although they use the same signal transduction network.
Molecular Immunology Unit, Max-Planck-Institut für Immunbiologie, Freiburg, Germany.
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WW
Schamel
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TP
Dick
D000818:Animals; D066246:ErbB Receptors / Q000502:physiology; D006133:Growth Substances / Q000502:physiology*; D008954:Models, Biological; D009154:Mutation; D016571:Neural Networks, Computer; D016716:PC12 Cells; D051381:Rats; D020794:Receptor Protein-Tyrosine Kinases / Q000235:genetics / Q000502:physiology; D017475:Receptors, Nerve Growth Factor / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology*
D006133:Growth Substances; D017475:Receptors, Nerve Growth Factor; D066246:ErbB Receptors; D020794:Receptor Protein-Tyrosine Kinases