Acetylation‐dependent oncogenic activity of metastasis‐associated protein 1 co‐regulator
Abstract High expression of metastasis‐associated protein 1 co‐regulator (MTA1), a component of the nuclear remodelling and histone deacetylase complex, has been associated with human tumours. However, the precise role of MTA1 in tumorigenesis remains unknown. In this study, we show that induced lev...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Ohshiro, Kazufumi [verfasserIn] Rayala, Suresh K [verfasserIn] Wigerup, Caroline [verfasserIn] Pakala, Suresh B [verfasserIn] Natha, Reddy S Divijendra [verfasserIn] Gururaj, Anupama E [verfasserIn] Molli, Poonam R [verfasserIn] Månsson, Sofie Svensson [verfasserIn] Ramezani, Ali [verfasserIn] Hawley, Robert G [verfasserIn] Landberg, Goran [verfasserIn] Lee, Norman H [verfasserIn] Kumar, Rakesh [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2010 |
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| Schlagwörter: |
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| Anmerkung: |
© European Molecular Biology Organization 2010 |
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| Übergeordnetes Werk: |
Enthalten in: EMBO Reports - Nature Publishing Group UK, 2023, 11(2010), 9 vom: 23. Juli, Seite 691-697 |
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| Übergeordnetes Werk: |
volume:11 ; year:2010 ; number:9 ; day:23 ; month:07 ; pages:691-697 |
| Links: |
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| DOI / URN: |
10.1038/embor.2010.99 |
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| Katalog-ID: |
SPR058083057 |
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| 245 | 1 | 0 | |a Acetylation‐dependent oncogenic activity of metastasis‐associated protein 1 co‐regulator |
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| 520 | |a Abstract High expression of metastasis‐associated protein 1 co‐regulator (MTA1), a component of the nuclear remodelling and histone deacetylase complex, has been associated with human tumours. However, the precise role of MTA1 in tumorigenesis remains unknown. In this study, we show that induced levels of MTA1 are sufficient to transform Rat1 fibroblasts and that the transforming potential of MTA1 is dependent on its acetylation at Lys626. Underlying mechanisms of MTA1‐mediated transformation include activation of the Ras–Raf pathway by MTA1 but not by acetylation‐inactive MTA1; this was due to the repression of Gαi2 transcription, which negatively influences Ras activation. We observed that acetylated MTA1–histone deacetylase (HDAC) interaction was required for the recruitment of the MTA1–HDAC complex to the Gαi2 regulatory element and consequently for the repression of Gαi2 transcription and expression leading to activation of the Ras–Raf pathway. The findings presented in this study provide for the first time—to the best of our knowledge—evidence of acetylation‐dependent oncogenic activity of a cancer‐relevant gene product. | ||
| 520 | |a Abstract MTA overexpression has been linked to cancer progression. This study indicates that Lys 626 acetylation of MTA1 is essential for the activation of the Ras–Raf pathway, which mediates the transforming activity of MTA1. | ||
| 650 | 4 | |a MTA1 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Lys 626 acetylation |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Raf1 activation |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Ras |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a transformation |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Rayala, Suresh K |e verfasserin |4 aut | |
| 700 | 1 | |a Wigerup, Caroline |e verfasserin |4 aut | |
| 700 | 1 | |a Pakala, Suresh B |e verfasserin |4 aut | |
| 700 | 1 | |a Natha, Reddy S Divijendra |e verfasserin |4 aut | |
| 700 | 1 | |a Gururaj, Anupama E |e verfasserin |4 aut | |
| 700 | 1 | |a Molli, Poonam R |e verfasserin |4 aut | |
| 700 | 1 | |a Månsson, Sofie Svensson |e verfasserin |4 aut | |
| 700 | 1 | |a Ramezani, Ali |e verfasserin |4 aut | |
| 700 | 1 | |a Hawley, Robert G |e verfasserin |4 aut | |
| 700 | 1 | |a Landberg, Goran |e verfasserin |4 aut | |
| 700 | 1 | |a Lee, Norman H |e verfasserin |4 aut | |
| 700 | 1 | |a Kumar, Rakesh |e verfasserin |4 aut | |
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10.1038/embor.2010.99 doi (DE-627)SPR058083057 (SPR)embor.2010.99-e DE-627 ger DE-627 rakwb eng Ohshiro, Kazufumi verfasserin aut Acetylation‐dependent oncogenic activity of metastasis‐associated protein 1 co‐regulator 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2010 Abstract High expression of metastasis‐associated protein 1 co‐regulator (MTA1), a component of the nuclear remodelling and histone deacetylase complex, has been associated with human tumours. However, the precise role of MTA1 in tumorigenesis remains unknown. In this study, we show that induced levels of MTA1 are sufficient to transform Rat1 fibroblasts and that the transforming potential of MTA1 is dependent on its acetylation at Lys626. Underlying mechanisms of MTA1‐mediated transformation include activation of the Ras–Raf pathway by MTA1 but not by acetylation‐inactive MTA1; this was due to the repression of Gαi2 transcription, which negatively influences Ras activation. We observed that acetylated MTA1–histone deacetylase (HDAC) interaction was required for the recruitment of the MTA1–HDAC complex to the Gαi2 regulatory element and consequently for the repression of Gαi2 transcription and expression leading to activation of the Ras–Raf pathway. The findings presented in this study provide for the first time—to the best of our knowledge—evidence of acetylation‐dependent oncogenic activity of a cancer‐relevant gene product. Abstract MTA overexpression has been linked to cancer progression. This study indicates that Lys 626 acetylation of MTA1 is essential for the activation of the Ras–Raf pathway, which mediates the transforming activity of MTA1. MTA1 (dpeaa)DE-He213 Lys 626 acetylation (dpeaa)DE-He213 Raf1 activation (dpeaa)DE-He213 Ras (dpeaa)DE-He213 transformation (dpeaa)DE-He213 Rayala, Suresh K verfasserin aut Wigerup, Caroline verfasserin aut Pakala, Suresh B verfasserin aut Natha, Reddy S Divijendra verfasserin aut Gururaj, Anupama E verfasserin aut Molli, Poonam R verfasserin aut Månsson, Sofie Svensson verfasserin aut Ramezani, Ali verfasserin aut Hawley, Robert G verfasserin aut Landberg, Goran verfasserin aut Lee, Norman H verfasserin aut Kumar, Rakesh verfasserin aut Enthalten in EMBO Reports Nature Publishing Group UK, 2023 11(2010), 9 vom: 23. Juli, Seite 691-697 (DE-627)320645622 (DE-600)2025376-X 1469-3178 nnns volume:11 year:2010 number:9 day:23 month:07 pages:691-697 https://dx.doi.org/10.1038/embor.2010.99 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_11 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_60 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_370 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_4116 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_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 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_4598 GBV_ILN_4700 AR 11 2010 9 23 07 691-697 |
| spelling |
10.1038/embor.2010.99 doi (DE-627)SPR058083057 (SPR)embor.2010.99-e DE-627 ger DE-627 rakwb eng Ohshiro, Kazufumi verfasserin aut Acetylation‐dependent oncogenic activity of metastasis‐associated protein 1 co‐regulator 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2010 Abstract High expression of metastasis‐associated protein 1 co‐regulator (MTA1), a component of the nuclear remodelling and histone deacetylase complex, has been associated with human tumours. However, the precise role of MTA1 in tumorigenesis remains unknown. In this study, we show that induced levels of MTA1 are sufficient to transform Rat1 fibroblasts and that the transforming potential of MTA1 is dependent on its acetylation at Lys626. Underlying mechanisms of MTA1‐mediated transformation include activation of the Ras–Raf pathway by MTA1 but not by acetylation‐inactive MTA1; this was due to the repression of Gαi2 transcription, which negatively influences Ras activation. We observed that acetylated MTA1–histone deacetylase (HDAC) interaction was required for the recruitment of the MTA1–HDAC complex to the Gαi2 regulatory element and consequently for the repression of Gαi2 transcription and expression leading to activation of the Ras–Raf pathway. The findings presented in this study provide for the first time—to the best of our knowledge—evidence of acetylation‐dependent oncogenic activity of a cancer‐relevant gene product. Abstract MTA overexpression has been linked to cancer progression. This study indicates that Lys 626 acetylation of MTA1 is essential for the activation of the Ras–Raf pathway, which mediates the transforming activity of MTA1. MTA1 (dpeaa)DE-He213 Lys 626 acetylation (dpeaa)DE-He213 Raf1 activation (dpeaa)DE-He213 Ras (dpeaa)DE-He213 transformation (dpeaa)DE-He213 Rayala, Suresh K verfasserin aut Wigerup, Caroline verfasserin aut Pakala, Suresh B verfasserin aut Natha, Reddy S Divijendra verfasserin aut Gururaj, Anupama E verfasserin aut Molli, Poonam R verfasserin aut Månsson, Sofie Svensson verfasserin aut Ramezani, Ali verfasserin aut Hawley, Robert G verfasserin aut Landberg, Goran verfasserin aut Lee, Norman H verfasserin aut Kumar, Rakesh verfasserin aut Enthalten in EMBO Reports Nature Publishing Group UK, 2023 11(2010), 9 vom: 23. Juli, Seite 691-697 (DE-627)320645622 (DE-600)2025376-X 1469-3178 nnns volume:11 year:2010 number:9 day:23 month:07 pages:691-697 https://dx.doi.org/10.1038/embor.2010.99 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_11 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_60 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_370 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_4116 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_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 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_4598 GBV_ILN_4700 AR 11 2010 9 23 07 691-697 |
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10.1038/embor.2010.99 doi (DE-627)SPR058083057 (SPR)embor.2010.99-e DE-627 ger DE-627 rakwb eng Ohshiro, Kazufumi verfasserin aut Acetylation‐dependent oncogenic activity of metastasis‐associated protein 1 co‐regulator 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2010 Abstract High expression of metastasis‐associated protein 1 co‐regulator (MTA1), a component of the nuclear remodelling and histone deacetylase complex, has been associated with human tumours. However, the precise role of MTA1 in tumorigenesis remains unknown. In this study, we show that induced levels of MTA1 are sufficient to transform Rat1 fibroblasts and that the transforming potential of MTA1 is dependent on its acetylation at Lys626. Underlying mechanisms of MTA1‐mediated transformation include activation of the Ras–Raf pathway by MTA1 but not by acetylation‐inactive MTA1; this was due to the repression of Gαi2 transcription, which negatively influences Ras activation. We observed that acetylated MTA1–histone deacetylase (HDAC) interaction was required for the recruitment of the MTA1–HDAC complex to the Gαi2 regulatory element and consequently for the repression of Gαi2 transcription and expression leading to activation of the Ras–Raf pathway. The findings presented in this study provide for the first time—to the best of our knowledge—evidence of acetylation‐dependent oncogenic activity of a cancer‐relevant gene product. Abstract MTA overexpression has been linked to cancer progression. This study indicates that Lys 626 acetylation of MTA1 is essential for the activation of the Ras–Raf pathway, which mediates the transforming activity of MTA1. MTA1 (dpeaa)DE-He213 Lys 626 acetylation (dpeaa)DE-He213 Raf1 activation (dpeaa)DE-He213 Ras (dpeaa)DE-He213 transformation (dpeaa)DE-He213 Rayala, Suresh K verfasserin aut Wigerup, Caroline verfasserin aut Pakala, Suresh B verfasserin aut Natha, Reddy S Divijendra verfasserin aut Gururaj, Anupama E verfasserin aut Molli, Poonam R verfasserin aut Månsson, Sofie Svensson verfasserin aut Ramezani, Ali verfasserin aut Hawley, Robert G verfasserin aut Landberg, Goran verfasserin aut Lee, Norman H verfasserin aut Kumar, Rakesh verfasserin aut Enthalten in EMBO Reports Nature Publishing Group UK, 2023 11(2010), 9 vom: 23. Juli, Seite 691-697 (DE-627)320645622 (DE-600)2025376-X 1469-3178 nnns volume:11 year:2010 number:9 day:23 month:07 pages:691-697 https://dx.doi.org/10.1038/embor.2010.99 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_11 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_60 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_370 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_4116 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_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 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_4598 GBV_ILN_4700 AR 11 2010 9 23 07 691-697 |
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10.1038/embor.2010.99 doi (DE-627)SPR058083057 (SPR)embor.2010.99-e DE-627 ger DE-627 rakwb eng Ohshiro, Kazufumi verfasserin aut Acetylation‐dependent oncogenic activity of metastasis‐associated protein 1 co‐regulator 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2010 Abstract High expression of metastasis‐associated protein 1 co‐regulator (MTA1), a component of the nuclear remodelling and histone deacetylase complex, has been associated with human tumours. However, the precise role of MTA1 in tumorigenesis remains unknown. In this study, we show that induced levels of MTA1 are sufficient to transform Rat1 fibroblasts and that the transforming potential of MTA1 is dependent on its acetylation at Lys626. Underlying mechanisms of MTA1‐mediated transformation include activation of the Ras–Raf pathway by MTA1 but not by acetylation‐inactive MTA1; this was due to the repression of Gαi2 transcription, which negatively influences Ras activation. We observed that acetylated MTA1–histone deacetylase (HDAC) interaction was required for the recruitment of the MTA1–HDAC complex to the Gαi2 regulatory element and consequently for the repression of Gαi2 transcription and expression leading to activation of the Ras–Raf pathway. The findings presented in this study provide for the first time—to the best of our knowledge—evidence of acetylation‐dependent oncogenic activity of a cancer‐relevant gene product. Abstract MTA overexpression has been linked to cancer progression. This study indicates that Lys 626 acetylation of MTA1 is essential for the activation of the Ras–Raf pathway, which mediates the transforming activity of MTA1. MTA1 (dpeaa)DE-He213 Lys 626 acetylation (dpeaa)DE-He213 Raf1 activation (dpeaa)DE-He213 Ras (dpeaa)DE-He213 transformation (dpeaa)DE-He213 Rayala, Suresh K verfasserin aut Wigerup, Caroline verfasserin aut Pakala, Suresh B verfasserin aut Natha, Reddy S Divijendra verfasserin aut Gururaj, Anupama E verfasserin aut Molli, Poonam R verfasserin aut Månsson, Sofie Svensson verfasserin aut Ramezani, Ali verfasserin aut Hawley, Robert G verfasserin aut Landberg, Goran verfasserin aut Lee, Norman H verfasserin aut Kumar, Rakesh verfasserin aut Enthalten in EMBO Reports Nature Publishing Group UK, 2023 11(2010), 9 vom: 23. Juli, Seite 691-697 (DE-627)320645622 (DE-600)2025376-X 1469-3178 nnns volume:11 year:2010 number:9 day:23 month:07 pages:691-697 https://dx.doi.org/10.1038/embor.2010.99 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_11 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_60 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_370 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_4116 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_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 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_4598 GBV_ILN_4700 AR 11 2010 9 23 07 691-697 |
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10.1038/embor.2010.99 doi (DE-627)SPR058083057 (SPR)embor.2010.99-e DE-627 ger DE-627 rakwb eng Ohshiro, Kazufumi verfasserin aut Acetylation‐dependent oncogenic activity of metastasis‐associated protein 1 co‐regulator 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2010 Abstract High expression of metastasis‐associated protein 1 co‐regulator (MTA1), a component of the nuclear remodelling and histone deacetylase complex, has been associated with human tumours. However, the precise role of MTA1 in tumorigenesis remains unknown. In this study, we show that induced levels of MTA1 are sufficient to transform Rat1 fibroblasts and that the transforming potential of MTA1 is dependent on its acetylation at Lys626. Underlying mechanisms of MTA1‐mediated transformation include activation of the Ras–Raf pathway by MTA1 but not by acetylation‐inactive MTA1; this was due to the repression of Gαi2 transcription, which negatively influences Ras activation. We observed that acetylated MTA1–histone deacetylase (HDAC) interaction was required for the recruitment of the MTA1–HDAC complex to the Gαi2 regulatory element and consequently for the repression of Gαi2 transcription and expression leading to activation of the Ras–Raf pathway. The findings presented in this study provide for the first time—to the best of our knowledge—evidence of acetylation‐dependent oncogenic activity of a cancer‐relevant gene product. Abstract MTA overexpression has been linked to cancer progression. This study indicates that Lys 626 acetylation of MTA1 is essential for the activation of the Ras–Raf pathway, which mediates the transforming activity of MTA1. MTA1 (dpeaa)DE-He213 Lys 626 acetylation (dpeaa)DE-He213 Raf1 activation (dpeaa)DE-He213 Ras (dpeaa)DE-He213 transformation (dpeaa)DE-He213 Rayala, Suresh K verfasserin aut Wigerup, Caroline verfasserin aut Pakala, Suresh B verfasserin aut Natha, Reddy S Divijendra verfasserin aut Gururaj, Anupama E verfasserin aut Molli, Poonam R verfasserin aut Månsson, Sofie Svensson verfasserin aut Ramezani, Ali verfasserin aut Hawley, Robert G verfasserin aut Landberg, Goran verfasserin aut Lee, Norman H verfasserin aut Kumar, Rakesh verfasserin aut Enthalten in EMBO Reports Nature Publishing Group UK, 2023 11(2010), 9 vom: 23. Juli, Seite 691-697 (DE-627)320645622 (DE-600)2025376-X 1469-3178 nnns volume:11 year:2010 number:9 day:23 month:07 pages:691-697 https://dx.doi.org/10.1038/embor.2010.99 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_11 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_60 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_370 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_4116 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_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 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_4598 GBV_ILN_4700 AR 11 2010 9 23 07 691-697 |
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Enthalten in EMBO Reports 11(2010), 9 vom: 23. Juli, Seite 691-697 volume:11 year:2010 number:9 day:23 month:07 pages:691-697 |
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Enthalten in EMBO Reports 11(2010), 9 vom: 23. Juli, Seite 691-697 volume:11 year:2010 number:9 day:23 month:07 pages:691-697 |
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MTA1 Lys 626 acetylation Raf1 activation Ras transformation |
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Ohshiro, Kazufumi @@aut@@ Rayala, Suresh K @@aut@@ Wigerup, Caroline @@aut@@ Pakala, Suresh B @@aut@@ Natha, Reddy S Divijendra @@aut@@ Gururaj, Anupama E @@aut@@ Molli, Poonam R @@aut@@ Månsson, Sofie Svensson @@aut@@ Ramezani, Ali @@aut@@ Hawley, Robert G @@aut@@ Landberg, Goran @@aut@@ Lee, Norman H @@aut@@ Kumar, Rakesh @@aut@@ |
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2010-07-23T00:00:00Z |
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However, the precise role of MTA1 in tumorigenesis remains unknown. In this study, we show that induced levels of MTA1 are sufficient to transform Rat1 fibroblasts and that the transforming potential of MTA1 is dependent on its acetylation at Lys626. Underlying mechanisms of MTA1‐mediated transformation include activation of the Ras–Raf pathway by MTA1 but not by acetylation‐inactive MTA1; this was due to the repression of Gαi2 transcription, which negatively influences Ras activation. We observed that acetylated MTA1–histone deacetylase (HDAC) interaction was required for the recruitment of the MTA1–HDAC complex to the Gαi2 regulatory element and consequently for the repression of Gαi2 transcription and expression leading to activation of the Ras–Raf pathway. 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Ohshiro, Kazufumi |
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Ohshiro, Kazufumi misc MTA1 misc Lys 626 acetylation misc Raf1 activation misc Ras misc transformation Acetylation‐dependent oncogenic activity of metastasis‐associated protein 1 co‐regulator |
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Acetylation‐dependent oncogenic activity of metastasis‐associated protein 1 co‐regulator MTA1 (dpeaa)DE-He213 Lys 626 acetylation (dpeaa)DE-He213 Raf1 activation (dpeaa)DE-He213 Ras (dpeaa)DE-He213 transformation (dpeaa)DE-He213 |
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Acetylation‐dependent oncogenic activity of metastasis‐associated protein 1 co‐regulator |
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Acetylation‐dependent oncogenic activity of metastasis‐associated protein 1 co‐regulator |
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Ohshiro, Kazufumi |
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Ohshiro, Kazufumi Rayala, Suresh K Wigerup, Caroline Pakala, Suresh B Natha, Reddy S Divijendra Gururaj, Anupama E Molli, Poonam R Månsson, Sofie Svensson Ramezani, Ali Hawley, Robert G Landberg, Goran Lee, Norman H Kumar, Rakesh |
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Elektronische Aufsätze |
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Ohshiro, Kazufumi |
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10.1038/embor.2010.99 |
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acetylation‐dependent oncogenic activity of metastasis‐associated protein 1 co‐regulator |
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Acetylation‐dependent oncogenic activity of metastasis‐associated protein 1 co‐regulator |
| abstract |
Abstract High expression of metastasis‐associated protein 1 co‐regulator (MTA1), a component of the nuclear remodelling and histone deacetylase complex, has been associated with human tumours. However, the precise role of MTA1 in tumorigenesis remains unknown. In this study, we show that induced levels of MTA1 are sufficient to transform Rat1 fibroblasts and that the transforming potential of MTA1 is dependent on its acetylation at Lys626. Underlying mechanisms of MTA1‐mediated transformation include activation of the Ras–Raf pathway by MTA1 but not by acetylation‐inactive MTA1; this was due to the repression of Gαi2 transcription, which negatively influences Ras activation. We observed that acetylated MTA1–histone deacetylase (HDAC) interaction was required for the recruitment of the MTA1–HDAC complex to the Gαi2 regulatory element and consequently for the repression of Gαi2 transcription and expression leading to activation of the Ras–Raf pathway. The findings presented in this study provide for the first time—to the best of our knowledge—evidence of acetylation‐dependent oncogenic activity of a cancer‐relevant gene product. Abstract MTA overexpression has been linked to cancer progression. This study indicates that Lys 626 acetylation of MTA1 is essential for the activation of the Ras–Raf pathway, which mediates the transforming activity of MTA1. © European Molecular Biology Organization 2010 |
| abstractGer |
Abstract High expression of metastasis‐associated protein 1 co‐regulator (MTA1), a component of the nuclear remodelling and histone deacetylase complex, has been associated with human tumours. However, the precise role of MTA1 in tumorigenesis remains unknown. In this study, we show that induced levels of MTA1 are sufficient to transform Rat1 fibroblasts and that the transforming potential of MTA1 is dependent on its acetylation at Lys626. Underlying mechanisms of MTA1‐mediated transformation include activation of the Ras–Raf pathway by MTA1 but not by acetylation‐inactive MTA1; this was due to the repression of Gαi2 transcription, which negatively influences Ras activation. We observed that acetylated MTA1–histone deacetylase (HDAC) interaction was required for the recruitment of the MTA1–HDAC complex to the Gαi2 regulatory element and consequently for the repression of Gαi2 transcription and expression leading to activation of the Ras–Raf pathway. The findings presented in this study provide for the first time—to the best of our knowledge—evidence of acetylation‐dependent oncogenic activity of a cancer‐relevant gene product. Abstract MTA overexpression has been linked to cancer progression. This study indicates that Lys 626 acetylation of MTA1 is essential for the activation of the Ras–Raf pathway, which mediates the transforming activity of MTA1. © European Molecular Biology Organization 2010 |
| abstract_unstemmed |
Abstract High expression of metastasis‐associated protein 1 co‐regulator (MTA1), a component of the nuclear remodelling and histone deacetylase complex, has been associated with human tumours. However, the precise role of MTA1 in tumorigenesis remains unknown. In this study, we show that induced levels of MTA1 are sufficient to transform Rat1 fibroblasts and that the transforming potential of MTA1 is dependent on its acetylation at Lys626. Underlying mechanisms of MTA1‐mediated transformation include activation of the Ras–Raf pathway by MTA1 but not by acetylation‐inactive MTA1; this was due to the repression of Gαi2 transcription, which negatively influences Ras activation. We observed that acetylated MTA1–histone deacetylase (HDAC) interaction was required for the recruitment of the MTA1–HDAC complex to the Gαi2 regulatory element and consequently for the repression of Gαi2 transcription and expression leading to activation of the Ras–Raf pathway. The findings presented in this study provide for the first time—to the best of our knowledge—evidence of acetylation‐dependent oncogenic activity of a cancer‐relevant gene product. Abstract MTA overexpression has been linked to cancer progression. This study indicates that Lys 626 acetylation of MTA1 is essential for the activation of the Ras–Raf pathway, which mediates the transforming activity of MTA1. © European Molecular Biology Organization 2010 |
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Acetylation‐dependent oncogenic activity of metastasis‐associated protein 1 co‐regulator |
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Rayala, Suresh K Wigerup, Caroline Pakala, Suresh B Natha, Reddy S Divijendra Gururaj, Anupama E Molli, Poonam R Månsson, Sofie Svensson Ramezani, Ali Hawley, Robert G Landberg, Goran Lee, Norman H Kumar, Rakesh |
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| score |
7.3982754 |