dorsal/arxiv
View SchemaStress-induced rearrangements of cellular networks: consequences for protection and drug design
| Authors | Mate S. Szalay, Istvan A. Kovacs, Tamas Korcsmaros, Csaba Bode, Peter Csermely |
|---|---|
| Categories | |
| ArXiv ID | q-bio/0702006 |
| URL | https://arxiv.org/abs/q-bio/0702006 |
| DOI | 10.1016/j.febslet.2007.03.083 |
| Journal | FEBS Letters 581, 3675-3680 (2007) |
Abstract
The complexity of the cells can be described and understood by a number of networks such as protein-protein interaction, cytoskeletal, organelle, signalling, gene transcription and metabolic networks. All these networks are highly dynamic producing continuous rearrangements in their links, hubs, network-skeleton and modules. Here we describe the adaptation of cellular networks after various forms of stress causing perturbations, congestions and network damage. Chronic stress decreases link-density, decouples or even quarantines modules, and induces an increased competition between network hubs and bridges. Extremely long or strong stress may induce a topological phase transition in the respective cellular networks, which switches the cell to a completely different mode of cellular function. We summarize our initial knowledge on network restoration after stress including the role of molecular chaperones in this process. Finally, we discuss the implications of stress-induced network rearrangements in diseases and ageing, and propose therapeutic approaches both to increase the robustness and help the repair of cellular networks.
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"abstract": "The complexity of the cells can be described and understood by a number of\nnetworks such as protein-protein interaction, cytoskeletal, organelle,\nsignalling, gene transcription and metabolic networks. All these networks are\nhighly dynamic producing continuous rearrangements in their links, hubs,\nnetwork-skeleton and modules. Here we describe the adaptation of cellular\nnetworks after various forms of stress causing perturbations, congestions and\nnetwork damage. Chronic stress decreases link-density, decouples or even\nquarantines modules, and induces an increased competition between network hubs\nand bridges. Extremely long or strong stress may induce a topological phase\ntransition in the respective cellular networks, which switches the cell to a\ncompletely different mode of cellular function. We summarize our initial\nknowledge on network restoration after stress including the role of molecular\nchaperones in this process. Finally, we discuss the implications of\nstress-induced network rearrangements in diseases and ageing, and propose\ntherapeutic approaches both to increase the robustness and help the repair of\ncellular networks.",
"arxiv_id": "q-bio/0702006",
"authors": [
"Mate S. Szalay",
"Istvan A. Kovacs",
"Tamas Korcsmaros",
"Csaba Bode",
"Peter Csermely"
],
"categories": [
"q-bio.MN"
],
"doi": "10.1016/j.febslet.2007.03.083",
"journal_ref": "FEBS Letters 581, 3675-3680 (2007)",
"title": "Stress-induced rearrangements of cellular networks: consequences for protection and drug design",
"url": "https://arxiv.org/abs/q-bio/0702006"
},
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