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Stochastic effects as a force to increase the complexity of signaling networks

Cellular signaling networks are complex and appear to include many nonfunctional elements. Recently, it was suggested that nonfunctional interactions of proteins cause signaling noise, which, perhaps, shapes the signal transduction mechanism. However, the conditions under which molecular noise influ...

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Detalles Bibliográficos
Autores principales: Kuwahara, Hiroyuki, Gao, Xin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3725509/
https://www.ncbi.nlm.nih.gov/pubmed/23892365
http://dx.doi.org/10.1038/srep02297
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author Kuwahara, Hiroyuki
Gao, Xin
author_facet Kuwahara, Hiroyuki
Gao, Xin
author_sort Kuwahara, Hiroyuki
collection PubMed
description Cellular signaling networks are complex and appear to include many nonfunctional elements. Recently, it was suggested that nonfunctional interactions of proteins cause signaling noise, which, perhaps, shapes the signal transduction mechanism. However, the conditions under which molecular noise influences cellular information processing remain unclear. Here, we explore a large number of simple biological models of varying network sizes to understand the architectural conditions under which the interactions of signaling proteins can exhibit specific stochastic effects—called deviant effects—in which the average behavior of a biological system is substantially altered in the presence of molecular noise. We find that a small fraction of these networks does exhibit deviant effects and shares a common architectural feature whereas most of the networks show only insignificant levels of deviations. Interestingly, addition of seemingly unimportant interactions into protein networks gives rise to deviant effects.
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spelling pubmed-37255092013-07-29 Stochastic effects as a force to increase the complexity of signaling networks Kuwahara, Hiroyuki Gao, Xin Sci Rep Article Cellular signaling networks are complex and appear to include many nonfunctional elements. Recently, it was suggested that nonfunctional interactions of proteins cause signaling noise, which, perhaps, shapes the signal transduction mechanism. However, the conditions under which molecular noise influences cellular information processing remain unclear. Here, we explore a large number of simple biological models of varying network sizes to understand the architectural conditions under which the interactions of signaling proteins can exhibit specific stochastic effects—called deviant effects—in which the average behavior of a biological system is substantially altered in the presence of molecular noise. We find that a small fraction of these networks does exhibit deviant effects and shares a common architectural feature whereas most of the networks show only insignificant levels of deviations. Interestingly, addition of seemingly unimportant interactions into protein networks gives rise to deviant effects. Nature Publishing Group 2013-07-29 /pmc/articles/PMC3725509/ /pubmed/23892365 http://dx.doi.org/10.1038/srep02297 Text en Copyright © 2013, Macmillan Publishers Limited. All rights reserved http://creativecommons.org/licenses/by-nc-sa/3.0/ This work is licensed under a Creative Commons Attribution-NonCommercial-ShareALike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/
spellingShingle Article
Kuwahara, Hiroyuki
Gao, Xin
Stochastic effects as a force to increase the complexity of signaling networks
title Stochastic effects as a force to increase the complexity of signaling networks
title_full Stochastic effects as a force to increase the complexity of signaling networks
title_fullStr Stochastic effects as a force to increase the complexity of signaling networks
title_full_unstemmed Stochastic effects as a force to increase the complexity of signaling networks
title_short Stochastic effects as a force to increase the complexity of signaling networks
title_sort stochastic effects as a force to increase the complexity of signaling networks
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3725509/
https://www.ncbi.nlm.nih.gov/pubmed/23892365
http://dx.doi.org/10.1038/srep02297
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