Interaction of Axin and Dvl‐2 proteins regulates Dvl‐2‐stimulated TCF‐dependent transcription
Abstract Axin promotes the phosphorylation of β‐catenin by GSK‐3β, leading to β‐catenin degradation. Wnt signals interfere with β‐catenin turnover, resulting in enhanced transcription of target genes through the increased formation of β‐catenin complexes containing TCF transcription factors. Little...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Smalley, Matthew J. [verfasserIn] Sara, Elizabeth [verfasserIn] Paterson, Hugh [verfasserIn] Naylor, Stuart [verfasserIn] Cook, David [verfasserIn] Jayatilake, Hiran [verfasserIn] Fryer, Lee G. [verfasserIn] Hutchinson, Lisa [verfasserIn] Fry, Michael J. [verfasserIn] Dale, Trevor C. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1999 |
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| Schlagwörter: |
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| Anmerkung: |
© European Molecular Biology Organization 1999 |
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| Übergeordnetes Werk: |
Enthalten in: The EMBO Journal - Nature Publishing Group UK, 2023, 18(1999), 10 vom: 17. Mai, Seite 2823-2835 |
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| Übergeordnetes Werk: |
volume:18 ; year:1999 ; number:10 ; day:17 ; month:05 ; pages:2823-2835 |
| Links: |
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| DOI / URN: |
10.1093/emboj/18.10.2823 |
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| Katalog-ID: |
SPR057808554 |
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| 041 | |a eng | ||
| 100 | 1 | |a Smalley, Matthew J. |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Interaction of Axin and Dvl‐2 proteins regulates Dvl‐2‐stimulated TCF‐dependent transcription |
| 264 | 1 | |c 1999 | |
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| 500 | |a © European Molecular Biology Organization 1999 | ||
| 520 | |a Abstract Axin promotes the phosphorylation of β‐catenin by GSK‐3β, leading to β‐catenin degradation. Wnt signals interfere with β‐catenin turnover, resulting in enhanced transcription of target genes through the increased formation of β‐catenin complexes containing TCF transcription factors. Little is known about how GSK‐3β‐mediated β‐catenin turnover is regulated in response to Wnt signals. We have explored the relationship between Axin and Dvl‐2, a member of the Dishevelled family of proteins that function upstream of GSK‐3β. Expression of Dvl‐2 activated TCF‐dependent transcription. This was blocked by co‐expression of GSK‐3β or Axin. Expression of a 59 amino acid GSK‐3β‐binding region from Axin strongly activated transcription in the absence of an upstream signal. Introduction of a point mutation into full‐length Axin that prevented GSK‐3β binding also generated a transcriptional activator. When co‐expressed, Axin and Dvl‐2 co‐localized within expressing cells. When Dvl‐2 localization was altered using a C‐terminal CAAX motif, Axin was also redistributed, suggesting a close association between the two proteins, a conclusion supported by co‐immunoprecipitation data. Deletion analysis suggested that Dvl‐association determinants within Axin were contained between residues 603 and 810. The association of Axin with Dvl‐2 may be important in the transmission of Wnt signals from Dvl‐2 to GSK‐3β. | ||
| 650 | 4 | |a β‐catenin |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a GSK‐3β |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a localization |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a luciferase assay |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Sara, Elizabeth |e verfasserin |4 aut | |
| 700 | 1 | |a Paterson, Hugh |e verfasserin |4 aut | |
| 700 | 1 | |a Naylor, Stuart |e verfasserin |4 aut | |
| 700 | 1 | |a Cook, David |e verfasserin |4 aut | |
| 700 | 1 | |a Jayatilake, Hiran |e verfasserin |4 aut | |
| 700 | 1 | |a Fryer, Lee G. |e verfasserin |4 aut | |
| 700 | 1 | |a Hutchinson, Lisa |e verfasserin |4 aut | |
| 700 | 1 | |a Fry, Michael J. |e verfasserin |4 aut | |
| 700 | 1 | |a Dale, Trevor C. |e verfasserin |4 aut | |
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1999 |
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1999 |
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10.1093/emboj/18.10.2823 doi (DE-627)SPR057808554 (SPR)18.10.2823-e DE-627 ger DE-627 rakwb eng Smalley, Matthew J. verfasserin aut Interaction of Axin and Dvl‐2 proteins regulates Dvl‐2‐stimulated TCF‐dependent transcription 1999 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 1999 Abstract Axin promotes the phosphorylation of β‐catenin by GSK‐3β, leading to β‐catenin degradation. Wnt signals interfere with β‐catenin turnover, resulting in enhanced transcription of target genes through the increased formation of β‐catenin complexes containing TCF transcription factors. Little is known about how GSK‐3β‐mediated β‐catenin turnover is regulated in response to Wnt signals. We have explored the relationship between Axin and Dvl‐2, a member of the Dishevelled family of proteins that function upstream of GSK‐3β. Expression of Dvl‐2 activated TCF‐dependent transcription. This was blocked by co‐expression of GSK‐3β or Axin. Expression of a 59 amino acid GSK‐3β‐binding region from Axin strongly activated transcription in the absence of an upstream signal. Introduction of a point mutation into full‐length Axin that prevented GSK‐3β binding also generated a transcriptional activator. When co‐expressed, Axin and Dvl‐2 co‐localized within expressing cells. When Dvl‐2 localization was altered using a C‐terminal CAAX motif, Axin was also redistributed, suggesting a close association between the two proteins, a conclusion supported by co‐immunoprecipitation data. Deletion analysis suggested that Dvl‐association determinants within Axin were contained between residues 603 and 810. The association of Axin with Dvl‐2 may be important in the transmission of Wnt signals from Dvl‐2 to GSK‐3β. β‐catenin (dpeaa)DE-He213 GSK‐3β (dpeaa)DE-He213 localization (dpeaa)DE-He213 luciferase assay (dpeaa)DE-He213 Sara, Elizabeth verfasserin aut Paterson, Hugh verfasserin aut Naylor, Stuart verfasserin aut Cook, David verfasserin aut Jayatilake, Hiran verfasserin aut Fryer, Lee G. verfasserin aut Hutchinson, Lisa verfasserin aut Fry, Michael J. verfasserin aut Dale, Trevor C. verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 18(1999), 10 vom: 17. Mai, Seite 2823-2835 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:18 year:1999 number:10 day:17 month:05 pages:2823-2835 https://dx.doi.org/10.1093/emboj/18.10.2823 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 18 1999 10 17 05 2823-2835 |
| spelling |
10.1093/emboj/18.10.2823 doi (DE-627)SPR057808554 (SPR)18.10.2823-e DE-627 ger DE-627 rakwb eng Smalley, Matthew J. verfasserin aut Interaction of Axin and Dvl‐2 proteins regulates Dvl‐2‐stimulated TCF‐dependent transcription 1999 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 1999 Abstract Axin promotes the phosphorylation of β‐catenin by GSK‐3β, leading to β‐catenin degradation. Wnt signals interfere with β‐catenin turnover, resulting in enhanced transcription of target genes through the increased formation of β‐catenin complexes containing TCF transcription factors. Little is known about how GSK‐3β‐mediated β‐catenin turnover is regulated in response to Wnt signals. We have explored the relationship between Axin and Dvl‐2, a member of the Dishevelled family of proteins that function upstream of GSK‐3β. Expression of Dvl‐2 activated TCF‐dependent transcription. This was blocked by co‐expression of GSK‐3β or Axin. Expression of a 59 amino acid GSK‐3β‐binding region from Axin strongly activated transcription in the absence of an upstream signal. Introduction of a point mutation into full‐length Axin that prevented GSK‐3β binding also generated a transcriptional activator. When co‐expressed, Axin and Dvl‐2 co‐localized within expressing cells. When Dvl‐2 localization was altered using a C‐terminal CAAX motif, Axin was also redistributed, suggesting a close association between the two proteins, a conclusion supported by co‐immunoprecipitation data. Deletion analysis suggested that Dvl‐association determinants within Axin were contained between residues 603 and 810. The association of Axin with Dvl‐2 may be important in the transmission of Wnt signals from Dvl‐2 to GSK‐3β. β‐catenin (dpeaa)DE-He213 GSK‐3β (dpeaa)DE-He213 localization (dpeaa)DE-He213 luciferase assay (dpeaa)DE-He213 Sara, Elizabeth verfasserin aut Paterson, Hugh verfasserin aut Naylor, Stuart verfasserin aut Cook, David verfasserin aut Jayatilake, Hiran verfasserin aut Fryer, Lee G. verfasserin aut Hutchinson, Lisa verfasserin aut Fry, Michael J. verfasserin aut Dale, Trevor C. verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 18(1999), 10 vom: 17. Mai, Seite 2823-2835 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:18 year:1999 number:10 day:17 month:05 pages:2823-2835 https://dx.doi.org/10.1093/emboj/18.10.2823 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 18 1999 10 17 05 2823-2835 |
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10.1093/emboj/18.10.2823 doi (DE-627)SPR057808554 (SPR)18.10.2823-e DE-627 ger DE-627 rakwb eng Smalley, Matthew J. verfasserin aut Interaction of Axin and Dvl‐2 proteins regulates Dvl‐2‐stimulated TCF‐dependent transcription 1999 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 1999 Abstract Axin promotes the phosphorylation of β‐catenin by GSK‐3β, leading to β‐catenin degradation. Wnt signals interfere with β‐catenin turnover, resulting in enhanced transcription of target genes through the increased formation of β‐catenin complexes containing TCF transcription factors. Little is known about how GSK‐3β‐mediated β‐catenin turnover is regulated in response to Wnt signals. We have explored the relationship between Axin and Dvl‐2, a member of the Dishevelled family of proteins that function upstream of GSK‐3β. Expression of Dvl‐2 activated TCF‐dependent transcription. This was blocked by co‐expression of GSK‐3β or Axin. Expression of a 59 amino acid GSK‐3β‐binding region from Axin strongly activated transcription in the absence of an upstream signal. Introduction of a point mutation into full‐length Axin that prevented GSK‐3β binding also generated a transcriptional activator. When co‐expressed, Axin and Dvl‐2 co‐localized within expressing cells. When Dvl‐2 localization was altered using a C‐terminal CAAX motif, Axin was also redistributed, suggesting a close association between the two proteins, a conclusion supported by co‐immunoprecipitation data. Deletion analysis suggested that Dvl‐association determinants within Axin were contained between residues 603 and 810. The association of Axin with Dvl‐2 may be important in the transmission of Wnt signals from Dvl‐2 to GSK‐3β. β‐catenin (dpeaa)DE-He213 GSK‐3β (dpeaa)DE-He213 localization (dpeaa)DE-He213 luciferase assay (dpeaa)DE-He213 Sara, Elizabeth verfasserin aut Paterson, Hugh verfasserin aut Naylor, Stuart verfasserin aut Cook, David verfasserin aut Jayatilake, Hiran verfasserin aut Fryer, Lee G. verfasserin aut Hutchinson, Lisa verfasserin aut Fry, Michael J. verfasserin aut Dale, Trevor C. verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 18(1999), 10 vom: 17. Mai, Seite 2823-2835 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:18 year:1999 number:10 day:17 month:05 pages:2823-2835 https://dx.doi.org/10.1093/emboj/18.10.2823 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 18 1999 10 17 05 2823-2835 |
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10.1093/emboj/18.10.2823 doi (DE-627)SPR057808554 (SPR)18.10.2823-e DE-627 ger DE-627 rakwb eng Smalley, Matthew J. verfasserin aut Interaction of Axin and Dvl‐2 proteins regulates Dvl‐2‐stimulated TCF‐dependent transcription 1999 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 1999 Abstract Axin promotes the phosphorylation of β‐catenin by GSK‐3β, leading to β‐catenin degradation. Wnt signals interfere with β‐catenin turnover, resulting in enhanced transcription of target genes through the increased formation of β‐catenin complexes containing TCF transcription factors. Little is known about how GSK‐3β‐mediated β‐catenin turnover is regulated in response to Wnt signals. We have explored the relationship between Axin and Dvl‐2, a member of the Dishevelled family of proteins that function upstream of GSK‐3β. Expression of Dvl‐2 activated TCF‐dependent transcription. This was blocked by co‐expression of GSK‐3β or Axin. Expression of a 59 amino acid GSK‐3β‐binding region from Axin strongly activated transcription in the absence of an upstream signal. Introduction of a point mutation into full‐length Axin that prevented GSK‐3β binding also generated a transcriptional activator. When co‐expressed, Axin and Dvl‐2 co‐localized within expressing cells. When Dvl‐2 localization was altered using a C‐terminal CAAX motif, Axin was also redistributed, suggesting a close association between the two proteins, a conclusion supported by co‐immunoprecipitation data. Deletion analysis suggested that Dvl‐association determinants within Axin were contained between residues 603 and 810. The association of Axin with Dvl‐2 may be important in the transmission of Wnt signals from Dvl‐2 to GSK‐3β. β‐catenin (dpeaa)DE-He213 GSK‐3β (dpeaa)DE-He213 localization (dpeaa)DE-He213 luciferase assay (dpeaa)DE-He213 Sara, Elizabeth verfasserin aut Paterson, Hugh verfasserin aut Naylor, Stuart verfasserin aut Cook, David verfasserin aut Jayatilake, Hiran verfasserin aut Fryer, Lee G. verfasserin aut Hutchinson, Lisa verfasserin aut Fry, Michael J. verfasserin aut Dale, Trevor C. verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 18(1999), 10 vom: 17. Mai, Seite 2823-2835 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:18 year:1999 number:10 day:17 month:05 pages:2823-2835 https://dx.doi.org/10.1093/emboj/18.10.2823 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 18 1999 10 17 05 2823-2835 |
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10.1093/emboj/18.10.2823 doi (DE-627)SPR057808554 (SPR)18.10.2823-e DE-627 ger DE-627 rakwb eng Smalley, Matthew J. verfasserin aut Interaction of Axin and Dvl‐2 proteins regulates Dvl‐2‐stimulated TCF‐dependent transcription 1999 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 1999 Abstract Axin promotes the phosphorylation of β‐catenin by GSK‐3β, leading to β‐catenin degradation. Wnt signals interfere with β‐catenin turnover, resulting in enhanced transcription of target genes through the increased formation of β‐catenin complexes containing TCF transcription factors. Little is known about how GSK‐3β‐mediated β‐catenin turnover is regulated in response to Wnt signals. We have explored the relationship between Axin and Dvl‐2, a member of the Dishevelled family of proteins that function upstream of GSK‐3β. Expression of Dvl‐2 activated TCF‐dependent transcription. This was blocked by co‐expression of GSK‐3β or Axin. Expression of a 59 amino acid GSK‐3β‐binding region from Axin strongly activated transcription in the absence of an upstream signal. Introduction of a point mutation into full‐length Axin that prevented GSK‐3β binding also generated a transcriptional activator. When co‐expressed, Axin and Dvl‐2 co‐localized within expressing cells. When Dvl‐2 localization was altered using a C‐terminal CAAX motif, Axin was also redistributed, suggesting a close association between the two proteins, a conclusion supported by co‐immunoprecipitation data. Deletion analysis suggested that Dvl‐association determinants within Axin were contained between residues 603 and 810. The association of Axin with Dvl‐2 may be important in the transmission of Wnt signals from Dvl‐2 to GSK‐3β. β‐catenin (dpeaa)DE-He213 GSK‐3β (dpeaa)DE-He213 localization (dpeaa)DE-He213 luciferase assay (dpeaa)DE-He213 Sara, Elizabeth verfasserin aut Paterson, Hugh verfasserin aut Naylor, Stuart verfasserin aut Cook, David verfasserin aut Jayatilake, Hiran verfasserin aut Fryer, Lee G. verfasserin aut Hutchinson, Lisa verfasserin aut Fry, Michael J. verfasserin aut Dale, Trevor C. verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 18(1999), 10 vom: 17. Mai, Seite 2823-2835 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:18 year:1999 number:10 day:17 month:05 pages:2823-2835 https://dx.doi.org/10.1093/emboj/18.10.2823 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 18 1999 10 17 05 2823-2835 |
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Enthalten in The EMBO Journal 18(1999), 10 vom: 17. Mai, Seite 2823-2835 volume:18 year:1999 number:10 day:17 month:05 pages:2823-2835 |
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Enthalten in The EMBO Journal 18(1999), 10 vom: 17. Mai, Seite 2823-2835 volume:18 year:1999 number:10 day:17 month:05 pages:2823-2835 |
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Smalley, Matthew J. @@aut@@ Sara, Elizabeth @@aut@@ Paterson, Hugh @@aut@@ Naylor, Stuart @@aut@@ Cook, David @@aut@@ Jayatilake, Hiran @@aut@@ Fryer, Lee G. @@aut@@ Hutchinson, Lisa @@aut@@ Fry, Michael J. @@aut@@ Dale, Trevor C. @@aut@@ |
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Wnt signals interfere with β‐catenin turnover, resulting in enhanced transcription of target genes through the increased formation of β‐catenin complexes containing TCF transcription factors. Little is known about how GSK‐3β‐mediated β‐catenin turnover is regulated in response to Wnt signals. We have explored the relationship between Axin and Dvl‐2, a member of the Dishevelled family of proteins that function upstream of GSK‐3β. Expression of Dvl‐2 activated TCF‐dependent transcription. This was blocked by co‐expression of GSK‐3β or Axin. Expression of a 59 amino acid GSK‐3β‐binding region from Axin strongly activated transcription in the absence of an upstream signal. Introduction of a point mutation into full‐length Axin that prevented GSK‐3β binding also generated a transcriptional activator. When co‐expressed, Axin and Dvl‐2 co‐localized within expressing cells. 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| author |
Smalley, Matthew J. |
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Smalley, Matthew J. misc β‐catenin misc GSK‐3β misc localization misc luciferase assay Interaction of Axin and Dvl‐2 proteins regulates Dvl‐2‐stimulated TCF‐dependent transcription |
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Interaction of Axin and Dvl‐2 proteins regulates Dvl‐2‐stimulated TCF‐dependent transcription β‐catenin (dpeaa)DE-He213 GSK‐3β (dpeaa)DE-He213 localization (dpeaa)DE-He213 luciferase assay (dpeaa)DE-He213 |
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misc β‐catenin misc GSK‐3β misc localization misc luciferase assay |
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Interaction of Axin and Dvl‐2 proteins regulates Dvl‐2‐stimulated TCF‐dependent transcription |
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Interaction of Axin and Dvl‐2 proteins regulates Dvl‐2‐stimulated TCF‐dependent transcription |
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Smalley, Matthew J. Sara, Elizabeth Paterson, Hugh Naylor, Stuart Cook, David Jayatilake, Hiran Fryer, Lee G. Hutchinson, Lisa Fry, Michael J. Dale, Trevor C. |
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Smalley, Matthew J. |
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verfasserin |
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interaction of axin and dvl‐2 proteins regulates dvl‐2‐stimulated tcf‐dependent transcription |
| title_auth |
Interaction of Axin and Dvl‐2 proteins regulates Dvl‐2‐stimulated TCF‐dependent transcription |
| abstract |
Abstract Axin promotes the phosphorylation of β‐catenin by GSK‐3β, leading to β‐catenin degradation. Wnt signals interfere with β‐catenin turnover, resulting in enhanced transcription of target genes through the increased formation of β‐catenin complexes containing TCF transcription factors. Little is known about how GSK‐3β‐mediated β‐catenin turnover is regulated in response to Wnt signals. We have explored the relationship between Axin and Dvl‐2, a member of the Dishevelled family of proteins that function upstream of GSK‐3β. Expression of Dvl‐2 activated TCF‐dependent transcription. This was blocked by co‐expression of GSK‐3β or Axin. Expression of a 59 amino acid GSK‐3β‐binding region from Axin strongly activated transcription in the absence of an upstream signal. Introduction of a point mutation into full‐length Axin that prevented GSK‐3β binding also generated a transcriptional activator. When co‐expressed, Axin and Dvl‐2 co‐localized within expressing cells. When Dvl‐2 localization was altered using a C‐terminal CAAX motif, Axin was also redistributed, suggesting a close association between the two proteins, a conclusion supported by co‐immunoprecipitation data. Deletion analysis suggested that Dvl‐association determinants within Axin were contained between residues 603 and 810. The association of Axin with Dvl‐2 may be important in the transmission of Wnt signals from Dvl‐2 to GSK‐3β. © European Molecular Biology Organization 1999 |
| abstractGer |
Abstract Axin promotes the phosphorylation of β‐catenin by GSK‐3β, leading to β‐catenin degradation. Wnt signals interfere with β‐catenin turnover, resulting in enhanced transcription of target genes through the increased formation of β‐catenin complexes containing TCF transcription factors. Little is known about how GSK‐3β‐mediated β‐catenin turnover is regulated in response to Wnt signals. We have explored the relationship between Axin and Dvl‐2, a member of the Dishevelled family of proteins that function upstream of GSK‐3β. Expression of Dvl‐2 activated TCF‐dependent transcription. This was blocked by co‐expression of GSK‐3β or Axin. Expression of a 59 amino acid GSK‐3β‐binding region from Axin strongly activated transcription in the absence of an upstream signal. Introduction of a point mutation into full‐length Axin that prevented GSK‐3β binding also generated a transcriptional activator. When co‐expressed, Axin and Dvl‐2 co‐localized within expressing cells. When Dvl‐2 localization was altered using a C‐terminal CAAX motif, Axin was also redistributed, suggesting a close association between the two proteins, a conclusion supported by co‐immunoprecipitation data. Deletion analysis suggested that Dvl‐association determinants within Axin were contained between residues 603 and 810. The association of Axin with Dvl‐2 may be important in the transmission of Wnt signals from Dvl‐2 to GSK‐3β. © European Molecular Biology Organization 1999 |
| abstract_unstemmed |
Abstract Axin promotes the phosphorylation of β‐catenin by GSK‐3β, leading to β‐catenin degradation. Wnt signals interfere with β‐catenin turnover, resulting in enhanced transcription of target genes through the increased formation of β‐catenin complexes containing TCF transcription factors. Little is known about how GSK‐3β‐mediated β‐catenin turnover is regulated in response to Wnt signals. We have explored the relationship between Axin and Dvl‐2, a member of the Dishevelled family of proteins that function upstream of GSK‐3β. Expression of Dvl‐2 activated TCF‐dependent transcription. This was blocked by co‐expression of GSK‐3β or Axin. Expression of a 59 amino acid GSK‐3β‐binding region from Axin strongly activated transcription in the absence of an upstream signal. Introduction of a point mutation into full‐length Axin that prevented GSK‐3β binding also generated a transcriptional activator. When co‐expressed, Axin and Dvl‐2 co‐localized within expressing cells. When Dvl‐2 localization was altered using a C‐terminal CAAX motif, Axin was also redistributed, suggesting a close association between the two proteins, a conclusion supported by co‐immunoprecipitation data. Deletion analysis suggested that Dvl‐association determinants within Axin were contained between residues 603 and 810. The association of Axin with Dvl‐2 may be important in the transmission of Wnt signals from Dvl‐2 to GSK‐3β. © European Molecular Biology Organization 1999 |
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Interaction of Axin and Dvl‐2 proteins regulates Dvl‐2‐stimulated TCF‐dependent transcription |
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https://dx.doi.org/10.1093/emboj/18.10.2823 |
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Sara, Elizabeth Paterson, Hugh Naylor, Stuart Cook, David Jayatilake, Hiran Fryer, Lee G. Hutchinson, Lisa Fry, Michael J. Dale, Trevor C. |
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Sara, Elizabeth Paterson, Hugh Naylor, Stuart Cook, David Jayatilake, Hiran Fryer, Lee G. Hutchinson, Lisa Fry, Michael J. Dale, Trevor C. |
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10.1093/emboj/18.10.2823 |
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2024-10-16T04:50:54.181Z |
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|
| score |
7.39935 |