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Kinetic mechanisms for overexpression insensitivity and oncogene cooperation
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Zeitschriftentitel: | FEBS Letters |
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Personen und Körperschaften: | , , |
In: | FEBS Letters, 583, 2009, 1, S. 93-96 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
Wiley
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Schlagwörter: |
author_facet |
Legewie, Stefan Sers, Christine Herzel, Hanspeter Legewie, Stefan Sers, Christine Herzel, Hanspeter |
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author |
Legewie, Stefan Sers, Christine Herzel, Hanspeter |
spellingShingle |
Legewie, Stefan Sers, Christine Herzel, Hanspeter FEBS Letters Kinetic mechanisms for overexpression insensitivity and oncogene cooperation Cell Biology Genetics Molecular Biology Biochemistry Structural Biology Biophysics |
author_sort |
legewie, stefan |
spelling |
Legewie, Stefan Sers, Christine Herzel, Hanspeter 0014-5793 1873-3468 Wiley Cell Biology Genetics Molecular Biology Biochemistry Structural Biology Biophysics http://dx.doi.org/10.1016/j.febslet.2008.11.027 <jats:p>Minor (5–10 fold) activation of mitogenic signalling cascades typically induces cell division upon extracellular stimulation and is sufficient to support tumourigenesis when permanently triggered by activating mutations. Surprisingly, even strong signalling protein overexpression usually does not trigger deregulated cell proliferation, suggesting that basal state signalling is insensitive to wildtype protein overexpression. Using kinetic modelling of the core Ras cycle, we show that basal RasGTP signalling can be insensitive to Ras overexpression and thus identify a possible tumour suppression mechanism. We further show how phenotypically silent overexpression events within signalling cascades cooperate to bring about carcinogenesis. Our analyses underscore the need for a systems level understanding of tumour formation.</jats:p> Kinetic mechanisms for overexpression insensitivity and oncogene cooperation FEBS Letters |
doi_str_mv |
10.1016/j.febslet.2008.11.027 |
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Biologie Chemie und Pharmazie Physik |
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Wiley, 2009 |
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Wiley, 2009 |
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2009 |
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Wiley |
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FEBS Letters |
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49 |
title |
Kinetic mechanisms for overexpression insensitivity and oncogene cooperation |
title_unstemmed |
Kinetic mechanisms for overexpression insensitivity and oncogene cooperation |
title_full |
Kinetic mechanisms for overexpression insensitivity and oncogene cooperation |
title_fullStr |
Kinetic mechanisms for overexpression insensitivity and oncogene cooperation |
title_full_unstemmed |
Kinetic mechanisms for overexpression insensitivity and oncogene cooperation |
title_short |
Kinetic mechanisms for overexpression insensitivity and oncogene cooperation |
title_sort |
kinetic mechanisms for overexpression insensitivity and oncogene cooperation |
topic |
Cell Biology Genetics Molecular Biology Biochemistry Structural Biology Biophysics |
url |
http://dx.doi.org/10.1016/j.febslet.2008.11.027 |
publishDate |
2009 |
physical |
93-96 |
description |
<jats:p>Minor (5–10 fold) activation of mitogenic signalling cascades typically induces cell division upon extracellular stimulation and is sufficient to support tumourigenesis when permanently triggered by activating mutations. Surprisingly, even strong signalling protein overexpression usually does not trigger deregulated cell proliferation, suggesting that basal state signalling is insensitive to wildtype protein overexpression. Using kinetic modelling of the core Ras cycle, we show that basal RasGTP signalling can be insensitive to Ras overexpression and thus identify a possible tumour suppression mechanism. We further show how phenotypically silent overexpression events within signalling cascades cooperate to bring about carcinogenesis. Our analyses underscore the need for a systems level understanding of tumour formation.</jats:p> |
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author | Legewie, Stefan, Sers, Christine, Herzel, Hanspeter |
author_facet | Legewie, Stefan, Sers, Christine, Herzel, Hanspeter, Legewie, Stefan, Sers, Christine, Herzel, Hanspeter |
author_sort | legewie, stefan |
container_issue | 1 |
container_start_page | 93 |
container_title | FEBS Letters |
container_volume | 583 |
description | <jats:p>Minor (5–10 fold) activation of mitogenic signalling cascades typically induces cell division upon extracellular stimulation and is sufficient to support tumourigenesis when permanently triggered by activating mutations. Surprisingly, even strong signalling protein overexpression usually does not trigger deregulated cell proliferation, suggesting that basal state signalling is insensitive to wildtype protein overexpression. Using kinetic modelling of the core Ras cycle, we show that basal RasGTP signalling can be insensitive to Ras overexpression and thus identify a possible tumour suppression mechanism. We further show how phenotypically silent overexpression events within signalling cascades cooperate to bring about carcinogenesis. Our analyses underscore the need for a systems level understanding of tumour formation.</jats:p> |
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id | ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTAxNi9qLmZlYnNsZXQuMjAwOC4xMS4wMjc |
imprint | Wiley, 2009 |
imprint_str_mv | Wiley, 2009 |
institution | DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1 |
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physical | 93-96 |
publishDate | 2009 |
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series | FEBS Letters |
source_id | 49 |
spelling | Legewie, Stefan Sers, Christine Herzel, Hanspeter 0014-5793 1873-3468 Wiley Cell Biology Genetics Molecular Biology Biochemistry Structural Biology Biophysics http://dx.doi.org/10.1016/j.febslet.2008.11.027 <jats:p>Minor (5–10 fold) activation of mitogenic signalling cascades typically induces cell division upon extracellular stimulation and is sufficient to support tumourigenesis when permanently triggered by activating mutations. Surprisingly, even strong signalling protein overexpression usually does not trigger deregulated cell proliferation, suggesting that basal state signalling is insensitive to wildtype protein overexpression. Using kinetic modelling of the core Ras cycle, we show that basal RasGTP signalling can be insensitive to Ras overexpression and thus identify a possible tumour suppression mechanism. We further show how phenotypically silent overexpression events within signalling cascades cooperate to bring about carcinogenesis. Our analyses underscore the need for a systems level understanding of tumour formation.</jats:p> Kinetic mechanisms for overexpression insensitivity and oncogene cooperation FEBS Letters |
spellingShingle | Legewie, Stefan, Sers, Christine, Herzel, Hanspeter, FEBS Letters, Kinetic mechanisms for overexpression insensitivity and oncogene cooperation, Cell Biology, Genetics, Molecular Biology, Biochemistry, Structural Biology, Biophysics |
title | Kinetic mechanisms for overexpression insensitivity and oncogene cooperation |
title_full | Kinetic mechanisms for overexpression insensitivity and oncogene cooperation |
title_fullStr | Kinetic mechanisms for overexpression insensitivity and oncogene cooperation |
title_full_unstemmed | Kinetic mechanisms for overexpression insensitivity and oncogene cooperation |
title_short | Kinetic mechanisms for overexpression insensitivity and oncogene cooperation |
title_sort | kinetic mechanisms for overexpression insensitivity and oncogene cooperation |
title_unstemmed | Kinetic mechanisms for overexpression insensitivity and oncogene cooperation |
topic | Cell Biology, Genetics, Molecular Biology, Biochemistry, Structural Biology, Biophysics |
url | http://dx.doi.org/10.1016/j.febslet.2008.11.027 |