Cross‐talk between Ras and Rho signalling pathways in transformation favours proliferation and increased motility
Abstract Transformation by oncogenic Ras requires the function of the Rho family GTPases. We find that Ras‐transformed cells have elevated levels of RhoA‐GTP, which functions to inhibit the expression of the cell cycle inhibitor p21/Waf1. These high levels of Rho‐GTP are not a direct consequence of...
Ausführliche Beschreibung
Autor*in: |
Sahai, Erik [verfasserIn] Olson, Michael F. [verfasserIn] Marshall, C. J. [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2001 |
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Schlagwörter: |
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Anmerkung: |
© European Molecular Biology Organization 2001 |
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Übergeordnetes Werk: |
Enthalten in: The EMBO Journal - Nature Publishing Group UK, 2023, 20(2001), 4 vom: 15. Feb., Seite 755-766 |
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Übergeordnetes Werk: |
volume:20 ; year:2001 ; number:4 ; day:15 ; month:02 ; pages:755-766 |
Links: |
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DOI / URN: |
10.1093/emboj/20.4.755 |
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Katalog-ID: |
SPR057854327 |
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245 | 1 | 0 | |a Cross‐talk between Ras and Rho signalling pathways in transformation favours proliferation and increased motility |
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520 | |a Abstract Transformation by oncogenic Ras requires the function of the Rho family GTPases. We find that Ras‐transformed cells have elevated levels of RhoA‐GTP, which functions to inhibit the expression of the cell cycle inhibitor p21/Waf1. These high levels of Rho‐GTP are not a direct consequence of Ras signalling but are selected for in response to sustained ERK–MAP kinase signalling. While the elevated levels of Rho‐GTP control the level of p21/Waf, they no longer regulate the formation of actin stress fibres in transformed cells. We show that the sustained ERK–MAP kinase signalling resulting from transformation by oncogenic Ras down‐regulates ROCK1 and Rho‐kinase, two Rho effectors required for actin stress fibre formation. The repression of Rho‐ dependent stress fibre formation by ERK–MAP kinase signalling contributes to the increased motility of Ras‐transformed fibroblasts. Overexpression of the ROCK target LIM kinase restores actin stress fibres and inhibits the motility of Ras‐transformed fibroblasts. We propose a model in which Ras and Rho signalling pathways cross‐talk to promote signalling pathways favouring transformation. | ||
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700 | 1 | |a Marshall, C. J. |e verfasserin |4 aut | |
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10.1093/emboj/20.4.755 doi (DE-627)SPR057854327 (SPR)20.4.755-e DE-627 ger DE-627 rakwb eng Sahai, Erik verfasserin aut Cross‐talk between Ras and Rho signalling pathways in transformation favours proliferation and increased motility 2001 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2001 Abstract Transformation by oncogenic Ras requires the function of the Rho family GTPases. We find that Ras‐transformed cells have elevated levels of RhoA‐GTP, which functions to inhibit the expression of the cell cycle inhibitor p21/Waf1. These high levels of Rho‐GTP are not a direct consequence of Ras signalling but are selected for in response to sustained ERK–MAP kinase signalling. While the elevated levels of Rho‐GTP control the level of p21/Waf, they no longer regulate the formation of actin stress fibres in transformed cells. We show that the sustained ERK–MAP kinase signalling resulting from transformation by oncogenic Ras down‐regulates ROCK1 and Rho‐kinase, two Rho effectors required for actin stress fibre formation. The repression of Rho‐ dependent stress fibre formation by ERK–MAP kinase signalling contributes to the increased motility of Ras‐transformed fibroblasts. Overexpression of the ROCK target LIM kinase restores actin stress fibres and inhibits the motility of Ras‐transformed fibroblasts. We propose a model in which Ras and Rho signalling pathways cross‐talk to promote signalling pathways favouring transformation. LIM kinase (dpeaa)DE-He213 MAP kinase (dpeaa)DE-He213 p21 (dpeaa)DE-He213 Ras (dpeaa)DE-He213 Rho (dpeaa)DE-He213 ROCK (dpeaa)DE-He213 Olson, Michael F. verfasserin aut Marshall, C. J. verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 20(2001), 4 vom: 15. Feb., Seite 755-766 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:20 year:2001 number:4 day:15 month:02 pages:755-766 https://dx.doi.org/10.1093/emboj/20.4.755 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 20 2001 4 15 02 755-766 |
spelling |
10.1093/emboj/20.4.755 doi (DE-627)SPR057854327 (SPR)20.4.755-e DE-627 ger DE-627 rakwb eng Sahai, Erik verfasserin aut Cross‐talk between Ras and Rho signalling pathways in transformation favours proliferation and increased motility 2001 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2001 Abstract Transformation by oncogenic Ras requires the function of the Rho family GTPases. We find that Ras‐transformed cells have elevated levels of RhoA‐GTP, which functions to inhibit the expression of the cell cycle inhibitor p21/Waf1. These high levels of Rho‐GTP are not a direct consequence of Ras signalling but are selected for in response to sustained ERK–MAP kinase signalling. While the elevated levels of Rho‐GTP control the level of p21/Waf, they no longer regulate the formation of actin stress fibres in transformed cells. We show that the sustained ERK–MAP kinase signalling resulting from transformation by oncogenic Ras down‐regulates ROCK1 and Rho‐kinase, two Rho effectors required for actin stress fibre formation. The repression of Rho‐ dependent stress fibre formation by ERK–MAP kinase signalling contributes to the increased motility of Ras‐transformed fibroblasts. Overexpression of the ROCK target LIM kinase restores actin stress fibres and inhibits the motility of Ras‐transformed fibroblasts. We propose a model in which Ras and Rho signalling pathways cross‐talk to promote signalling pathways favouring transformation. LIM kinase (dpeaa)DE-He213 MAP kinase (dpeaa)DE-He213 p21 (dpeaa)DE-He213 Ras (dpeaa)DE-He213 Rho (dpeaa)DE-He213 ROCK (dpeaa)DE-He213 Olson, Michael F. verfasserin aut Marshall, C. J. verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 20(2001), 4 vom: 15. Feb., Seite 755-766 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:20 year:2001 number:4 day:15 month:02 pages:755-766 https://dx.doi.org/10.1093/emboj/20.4.755 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 20 2001 4 15 02 755-766 |
allfields_unstemmed |
10.1093/emboj/20.4.755 doi (DE-627)SPR057854327 (SPR)20.4.755-e DE-627 ger DE-627 rakwb eng Sahai, Erik verfasserin aut Cross‐talk between Ras and Rho signalling pathways in transformation favours proliferation and increased motility 2001 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2001 Abstract Transformation by oncogenic Ras requires the function of the Rho family GTPases. We find that Ras‐transformed cells have elevated levels of RhoA‐GTP, which functions to inhibit the expression of the cell cycle inhibitor p21/Waf1. These high levels of Rho‐GTP are not a direct consequence of Ras signalling but are selected for in response to sustained ERK–MAP kinase signalling. While the elevated levels of Rho‐GTP control the level of p21/Waf, they no longer regulate the formation of actin stress fibres in transformed cells. We show that the sustained ERK–MAP kinase signalling resulting from transformation by oncogenic Ras down‐regulates ROCK1 and Rho‐kinase, two Rho effectors required for actin stress fibre formation. The repression of Rho‐ dependent stress fibre formation by ERK–MAP kinase signalling contributes to the increased motility of Ras‐transformed fibroblasts. Overexpression of the ROCK target LIM kinase restores actin stress fibres and inhibits the motility of Ras‐transformed fibroblasts. We propose a model in which Ras and Rho signalling pathways cross‐talk to promote signalling pathways favouring transformation. LIM kinase (dpeaa)DE-He213 MAP kinase (dpeaa)DE-He213 p21 (dpeaa)DE-He213 Ras (dpeaa)DE-He213 Rho (dpeaa)DE-He213 ROCK (dpeaa)DE-He213 Olson, Michael F. verfasserin aut Marshall, C. J. verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 20(2001), 4 vom: 15. Feb., Seite 755-766 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:20 year:2001 number:4 day:15 month:02 pages:755-766 https://dx.doi.org/10.1093/emboj/20.4.755 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 20 2001 4 15 02 755-766 |
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10.1093/emboj/20.4.755 doi (DE-627)SPR057854327 (SPR)20.4.755-e DE-627 ger DE-627 rakwb eng Sahai, Erik verfasserin aut Cross‐talk between Ras and Rho signalling pathways in transformation favours proliferation and increased motility 2001 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2001 Abstract Transformation by oncogenic Ras requires the function of the Rho family GTPases. We find that Ras‐transformed cells have elevated levels of RhoA‐GTP, which functions to inhibit the expression of the cell cycle inhibitor p21/Waf1. These high levels of Rho‐GTP are not a direct consequence of Ras signalling but are selected for in response to sustained ERK–MAP kinase signalling. While the elevated levels of Rho‐GTP control the level of p21/Waf, they no longer regulate the formation of actin stress fibres in transformed cells. We show that the sustained ERK–MAP kinase signalling resulting from transformation by oncogenic Ras down‐regulates ROCK1 and Rho‐kinase, two Rho effectors required for actin stress fibre formation. The repression of Rho‐ dependent stress fibre formation by ERK–MAP kinase signalling contributes to the increased motility of Ras‐transformed fibroblasts. Overexpression of the ROCK target LIM kinase restores actin stress fibres and inhibits the motility of Ras‐transformed fibroblasts. We propose a model in which Ras and Rho signalling pathways cross‐talk to promote signalling pathways favouring transformation. LIM kinase (dpeaa)DE-He213 MAP kinase (dpeaa)DE-He213 p21 (dpeaa)DE-He213 Ras (dpeaa)DE-He213 Rho (dpeaa)DE-He213 ROCK (dpeaa)DE-He213 Olson, Michael F. verfasserin aut Marshall, C. J. verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 20(2001), 4 vom: 15. Feb., Seite 755-766 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:20 year:2001 number:4 day:15 month:02 pages:755-766 https://dx.doi.org/10.1093/emboj/20.4.755 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 20 2001 4 15 02 755-766 |
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10.1093/emboj/20.4.755 doi (DE-627)SPR057854327 (SPR)20.4.755-e DE-627 ger DE-627 rakwb eng Sahai, Erik verfasserin aut Cross‐talk between Ras and Rho signalling pathways in transformation favours proliferation and increased motility 2001 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2001 Abstract Transformation by oncogenic Ras requires the function of the Rho family GTPases. We find that Ras‐transformed cells have elevated levels of RhoA‐GTP, which functions to inhibit the expression of the cell cycle inhibitor p21/Waf1. These high levels of Rho‐GTP are not a direct consequence of Ras signalling but are selected for in response to sustained ERK–MAP kinase signalling. While the elevated levels of Rho‐GTP control the level of p21/Waf, they no longer regulate the formation of actin stress fibres in transformed cells. We show that the sustained ERK–MAP kinase signalling resulting from transformation by oncogenic Ras down‐regulates ROCK1 and Rho‐kinase, two Rho effectors required for actin stress fibre formation. The repression of Rho‐ dependent stress fibre formation by ERK–MAP kinase signalling contributes to the increased motility of Ras‐transformed fibroblasts. Overexpression of the ROCK target LIM kinase restores actin stress fibres and inhibits the motility of Ras‐transformed fibroblasts. We propose a model in which Ras and Rho signalling pathways cross‐talk to promote signalling pathways favouring transformation. LIM kinase (dpeaa)DE-He213 MAP kinase (dpeaa)DE-He213 p21 (dpeaa)DE-He213 Ras (dpeaa)DE-He213 Rho (dpeaa)DE-He213 ROCK (dpeaa)DE-He213 Olson, Michael F. verfasserin aut Marshall, C. J. verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 20(2001), 4 vom: 15. Feb., Seite 755-766 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:20 year:2001 number:4 day:15 month:02 pages:755-766 https://dx.doi.org/10.1093/emboj/20.4.755 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 20 2001 4 15 02 755-766 |
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Sahai, Erik |
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Sahai, Erik misc LIM kinase misc MAP kinase misc p21 misc Ras misc Rho misc ROCK Cross‐talk between Ras and Rho signalling pathways in transformation favours proliferation and increased motility |
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Cross‐talk between Ras and Rho signalling pathways in transformation favours proliferation and increased motility LIM kinase (dpeaa)DE-He213 MAP kinase (dpeaa)DE-He213 p21 (dpeaa)DE-He213 Ras (dpeaa)DE-He213 Rho (dpeaa)DE-He213 ROCK (dpeaa)DE-He213 |
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Cross‐talk between Ras and Rho signalling pathways in transformation favours proliferation and increased motility |
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Cross‐talk between Ras and Rho signalling pathways in transformation favours proliferation and increased motility |
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cross‐talk between ras and rho signalling pathways in transformation favours proliferation and increased motility |
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Cross‐talk between Ras and Rho signalling pathways in transformation favours proliferation and increased motility |
abstract |
Abstract Transformation by oncogenic Ras requires the function of the Rho family GTPases. We find that Ras‐transformed cells have elevated levels of RhoA‐GTP, which functions to inhibit the expression of the cell cycle inhibitor p21/Waf1. These high levels of Rho‐GTP are not a direct consequence of Ras signalling but are selected for in response to sustained ERK–MAP kinase signalling. While the elevated levels of Rho‐GTP control the level of p21/Waf, they no longer regulate the formation of actin stress fibres in transformed cells. We show that the sustained ERK–MAP kinase signalling resulting from transformation by oncogenic Ras down‐regulates ROCK1 and Rho‐kinase, two Rho effectors required for actin stress fibre formation. The repression of Rho‐ dependent stress fibre formation by ERK–MAP kinase signalling contributes to the increased motility of Ras‐transformed fibroblasts. Overexpression of the ROCK target LIM kinase restores actin stress fibres and inhibits the motility of Ras‐transformed fibroblasts. We propose a model in which Ras and Rho signalling pathways cross‐talk to promote signalling pathways favouring transformation. © European Molecular Biology Organization 2001 |
abstractGer |
Abstract Transformation by oncogenic Ras requires the function of the Rho family GTPases. We find that Ras‐transformed cells have elevated levels of RhoA‐GTP, which functions to inhibit the expression of the cell cycle inhibitor p21/Waf1. These high levels of Rho‐GTP are not a direct consequence of Ras signalling but are selected for in response to sustained ERK–MAP kinase signalling. While the elevated levels of Rho‐GTP control the level of p21/Waf, they no longer regulate the formation of actin stress fibres in transformed cells. We show that the sustained ERK–MAP kinase signalling resulting from transformation by oncogenic Ras down‐regulates ROCK1 and Rho‐kinase, two Rho effectors required for actin stress fibre formation. The repression of Rho‐ dependent stress fibre formation by ERK–MAP kinase signalling contributes to the increased motility of Ras‐transformed fibroblasts. Overexpression of the ROCK target LIM kinase restores actin stress fibres and inhibits the motility of Ras‐transformed fibroblasts. We propose a model in which Ras and Rho signalling pathways cross‐talk to promote signalling pathways favouring transformation. © European Molecular Biology Organization 2001 |
abstract_unstemmed |
Abstract Transformation by oncogenic Ras requires the function of the Rho family GTPases. We find that Ras‐transformed cells have elevated levels of RhoA‐GTP, which functions to inhibit the expression of the cell cycle inhibitor p21/Waf1. These high levels of Rho‐GTP are not a direct consequence of Ras signalling but are selected for in response to sustained ERK–MAP kinase signalling. While the elevated levels of Rho‐GTP control the level of p21/Waf, they no longer regulate the formation of actin stress fibres in transformed cells. We show that the sustained ERK–MAP kinase signalling resulting from transformation by oncogenic Ras down‐regulates ROCK1 and Rho‐kinase, two Rho effectors required for actin stress fibre formation. The repression of Rho‐ dependent stress fibre formation by ERK–MAP kinase signalling contributes to the increased motility of Ras‐transformed fibroblasts. Overexpression of the ROCK target LIM kinase restores actin stress fibres and inhibits the motility of Ras‐transformed fibroblasts. We propose a model in which Ras and Rho signalling pathways cross‐talk to promote signalling pathways favouring transformation. © European Molecular Biology Organization 2001 |
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Cross‐talk between Ras and Rho signalling pathways in transformation favours proliferation and increased motility |
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We find that Ras‐transformed cells have elevated levels of RhoA‐GTP, which functions to inhibit the expression of the cell cycle inhibitor p21/Waf1. These high levels of Rho‐GTP are not a direct consequence of Ras signalling but are selected for in response to sustained ERK–MAP kinase signalling. While the elevated levels of Rho‐GTP control the level of p21/Waf, they no longer regulate the formation of actin stress fibres in transformed cells. We show that the sustained ERK–MAP kinase signalling resulting from transformation by oncogenic Ras down‐regulates ROCK1 and Rho‐kinase, two Rho effectors required for actin stress fibre formation. The repression of Rho‐ dependent stress fibre formation by ERK–MAP kinase signalling contributes to the increased motility of Ras‐transformed fibroblasts. Overexpression of the ROCK target LIM kinase restores actin stress fibres and inhibits the motility of Ras‐transformed fibroblasts. 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