Sterols regulate ER‐export dynamics of secretory cargo protein ts‐O45‐G
Abstract Alterations in endoplasmic reticulum (ER) cholesterol are fundamental for a variety of cellular processes such as the regulation of lipid homeostasis or efficient protein degradation. We show that reduced levels of cellular sterols cause a delayed ER‐to‐Golgi transport of the secretory carg...
Ausführliche Beschreibung
Autor*in: |
Runz, Heiko [verfasserIn] Miura, Kota [verfasserIn] Weiss, Matthias [verfasserIn] Pepperkok, Rainer [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2006 |
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Schlagwörter: |
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Anmerkung: |
© European Molecular Biology Organization 2006 |
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Übergeordnetes Werk: |
Enthalten in: The EMBO Journal - Nature Publishing Group UK, 2023, 25(2006), 13 vom: 22. Juni, Seite 2953-2965 |
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Übergeordnetes Werk: |
volume:25 ; year:2006 ; number:13 ; day:22 ; month:06 ; pages:2953-2965 |
Links: |
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DOI / URN: |
10.1038/sj.emboj.7601205 |
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Katalog-ID: |
SPR057952434 |
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520 | |a Abstract Alterations in endoplasmic reticulum (ER) cholesterol are fundamental for a variety of cellular processes such as the regulation of lipid homeostasis or efficient protein degradation. We show that reduced levels of cellular sterols cause a delayed ER‐to‐Golgi transport of the secretory cargo membrane protein ts‐O45‐G and a relocation to the ER of an endogenous protein cycling between the ER and the Golgi complex. Transport inhibition is characterized by a delay in the accumulation of ts‐O45‐G in ER‐exit sites (ERES) and correlates with a reduced mobility of ts‐O45‐G within ER membranes. A simple mathematical model describing the kinetics of ER‐exit predicts that reduced cargo loading to ERES and not the reduced mobility of ts‐O45‐G accounts for the delayed ER‐exit and arrival at the Golgi. Consistent with this, membrane turnover of the COPII component Sec23p is delayed in sterol‐depleted cells. Altogether, our results demonstrate the importance of sterol levels in COPII mediated ER‐export. | ||
650 | 4 | |a cholesterol |7 (dpeaa)DE-He213 | |
650 | 4 | |a ER exit sites |7 (dpeaa)DE-He213 | |
650 | 4 | |a membrane trafficking |7 (dpeaa)DE-He213 | |
650 | 4 | |a modelling |7 (dpeaa)DE-He213 | |
650 | 4 | |a photobleaching |7 (dpeaa)DE-He213 | |
700 | 1 | |a Miura, Kota |e verfasserin |4 aut | |
700 | 1 | |a Weiss, Matthias |e verfasserin |4 aut | |
700 | 1 | |a Pepperkok, Rainer |e verfasserin |4 aut | |
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10.1038/sj.emboj.7601205 doi (DE-627)SPR057952434 (SPR)sj.emboj.7601205-e DE-627 ger DE-627 rakwb eng Runz, Heiko verfasserin aut Sterols regulate ER‐export dynamics of secretory cargo protein ts‐O45‐G 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2006 Abstract Alterations in endoplasmic reticulum (ER) cholesterol are fundamental for a variety of cellular processes such as the regulation of lipid homeostasis or efficient protein degradation. We show that reduced levels of cellular sterols cause a delayed ER‐to‐Golgi transport of the secretory cargo membrane protein ts‐O45‐G and a relocation to the ER of an endogenous protein cycling between the ER and the Golgi complex. Transport inhibition is characterized by a delay in the accumulation of ts‐O45‐G in ER‐exit sites (ERES) and correlates with a reduced mobility of ts‐O45‐G within ER membranes. A simple mathematical model describing the kinetics of ER‐exit predicts that reduced cargo loading to ERES and not the reduced mobility of ts‐O45‐G accounts for the delayed ER‐exit and arrival at the Golgi. Consistent with this, membrane turnover of the COPII component Sec23p is delayed in sterol‐depleted cells. Altogether, our results demonstrate the importance of sterol levels in COPII mediated ER‐export. cholesterol (dpeaa)DE-He213 ER exit sites (dpeaa)DE-He213 membrane trafficking (dpeaa)DE-He213 modelling (dpeaa)DE-He213 photobleaching (dpeaa)DE-He213 Miura, Kota verfasserin aut Weiss, Matthias verfasserin aut Pepperkok, Rainer verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 25(2006), 13 vom: 22. Juni, Seite 2953-2965 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:25 year:2006 number:13 day:22 month:06 pages:2953-2965 https://dx.doi.org/10.1038/sj.emboj.7601205 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_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 25 2006 13 22 06 2953-2965 |
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10.1038/sj.emboj.7601205 doi (DE-627)SPR057952434 (SPR)sj.emboj.7601205-e DE-627 ger DE-627 rakwb eng Runz, Heiko verfasserin aut Sterols regulate ER‐export dynamics of secretory cargo protein ts‐O45‐G 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2006 Abstract Alterations in endoplasmic reticulum (ER) cholesterol are fundamental for a variety of cellular processes such as the regulation of lipid homeostasis or efficient protein degradation. We show that reduced levels of cellular sterols cause a delayed ER‐to‐Golgi transport of the secretory cargo membrane protein ts‐O45‐G and a relocation to the ER of an endogenous protein cycling between the ER and the Golgi complex. Transport inhibition is characterized by a delay in the accumulation of ts‐O45‐G in ER‐exit sites (ERES) and correlates with a reduced mobility of ts‐O45‐G within ER membranes. A simple mathematical model describing the kinetics of ER‐exit predicts that reduced cargo loading to ERES and not the reduced mobility of ts‐O45‐G accounts for the delayed ER‐exit and arrival at the Golgi. Consistent with this, membrane turnover of the COPII component Sec23p is delayed in sterol‐depleted cells. Altogether, our results demonstrate the importance of sterol levels in COPII mediated ER‐export. cholesterol (dpeaa)DE-He213 ER exit sites (dpeaa)DE-He213 membrane trafficking (dpeaa)DE-He213 modelling (dpeaa)DE-He213 photobleaching (dpeaa)DE-He213 Miura, Kota verfasserin aut Weiss, Matthias verfasserin aut Pepperkok, Rainer verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 25(2006), 13 vom: 22. Juni, Seite 2953-2965 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:25 year:2006 number:13 day:22 month:06 pages:2953-2965 https://dx.doi.org/10.1038/sj.emboj.7601205 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_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 25 2006 13 22 06 2953-2965 |
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10.1038/sj.emboj.7601205 doi (DE-627)SPR057952434 (SPR)sj.emboj.7601205-e DE-627 ger DE-627 rakwb eng Runz, Heiko verfasserin aut Sterols regulate ER‐export dynamics of secretory cargo protein ts‐O45‐G 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2006 Abstract Alterations in endoplasmic reticulum (ER) cholesterol are fundamental for a variety of cellular processes such as the regulation of lipid homeostasis or efficient protein degradation. We show that reduced levels of cellular sterols cause a delayed ER‐to‐Golgi transport of the secretory cargo membrane protein ts‐O45‐G and a relocation to the ER of an endogenous protein cycling between the ER and the Golgi complex. Transport inhibition is characterized by a delay in the accumulation of ts‐O45‐G in ER‐exit sites (ERES) and correlates with a reduced mobility of ts‐O45‐G within ER membranes. A simple mathematical model describing the kinetics of ER‐exit predicts that reduced cargo loading to ERES and not the reduced mobility of ts‐O45‐G accounts for the delayed ER‐exit and arrival at the Golgi. Consistent with this, membrane turnover of the COPII component Sec23p is delayed in sterol‐depleted cells. Altogether, our results demonstrate the importance of sterol levels in COPII mediated ER‐export. cholesterol (dpeaa)DE-He213 ER exit sites (dpeaa)DE-He213 membrane trafficking (dpeaa)DE-He213 modelling (dpeaa)DE-He213 photobleaching (dpeaa)DE-He213 Miura, Kota verfasserin aut Weiss, Matthias verfasserin aut Pepperkok, Rainer verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 25(2006), 13 vom: 22. Juni, Seite 2953-2965 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:25 year:2006 number:13 day:22 month:06 pages:2953-2965 https://dx.doi.org/10.1038/sj.emboj.7601205 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_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 25 2006 13 22 06 2953-2965 |
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10.1038/sj.emboj.7601205 doi (DE-627)SPR057952434 (SPR)sj.emboj.7601205-e DE-627 ger DE-627 rakwb eng Runz, Heiko verfasserin aut Sterols regulate ER‐export dynamics of secretory cargo protein ts‐O45‐G 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2006 Abstract Alterations in endoplasmic reticulum (ER) cholesterol are fundamental for a variety of cellular processes such as the regulation of lipid homeostasis or efficient protein degradation. We show that reduced levels of cellular sterols cause a delayed ER‐to‐Golgi transport of the secretory cargo membrane protein ts‐O45‐G and a relocation to the ER of an endogenous protein cycling between the ER and the Golgi complex. Transport inhibition is characterized by a delay in the accumulation of ts‐O45‐G in ER‐exit sites (ERES) and correlates with a reduced mobility of ts‐O45‐G within ER membranes. A simple mathematical model describing the kinetics of ER‐exit predicts that reduced cargo loading to ERES and not the reduced mobility of ts‐O45‐G accounts for the delayed ER‐exit and arrival at the Golgi. Consistent with this, membrane turnover of the COPII component Sec23p is delayed in sterol‐depleted cells. Altogether, our results demonstrate the importance of sterol levels in COPII mediated ER‐export. cholesterol (dpeaa)DE-He213 ER exit sites (dpeaa)DE-He213 membrane trafficking (dpeaa)DE-He213 modelling (dpeaa)DE-He213 photobleaching (dpeaa)DE-He213 Miura, Kota verfasserin aut Weiss, Matthias verfasserin aut Pepperkok, Rainer verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 25(2006), 13 vom: 22. Juni, Seite 2953-2965 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:25 year:2006 number:13 day:22 month:06 pages:2953-2965 https://dx.doi.org/10.1038/sj.emboj.7601205 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_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 25 2006 13 22 06 2953-2965 |
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10.1038/sj.emboj.7601205 doi (DE-627)SPR057952434 (SPR)sj.emboj.7601205-e DE-627 ger DE-627 rakwb eng Runz, Heiko verfasserin aut Sterols regulate ER‐export dynamics of secretory cargo protein ts‐O45‐G 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2006 Abstract Alterations in endoplasmic reticulum (ER) cholesterol are fundamental for a variety of cellular processes such as the regulation of lipid homeostasis or efficient protein degradation. We show that reduced levels of cellular sterols cause a delayed ER‐to‐Golgi transport of the secretory cargo membrane protein ts‐O45‐G and a relocation to the ER of an endogenous protein cycling between the ER and the Golgi complex. Transport inhibition is characterized by a delay in the accumulation of ts‐O45‐G in ER‐exit sites (ERES) and correlates with a reduced mobility of ts‐O45‐G within ER membranes. A simple mathematical model describing the kinetics of ER‐exit predicts that reduced cargo loading to ERES and not the reduced mobility of ts‐O45‐G accounts for the delayed ER‐exit and arrival at the Golgi. Consistent with this, membrane turnover of the COPII component Sec23p is delayed in sterol‐depleted cells. Altogether, our results demonstrate the importance of sterol levels in COPII mediated ER‐export. cholesterol (dpeaa)DE-He213 ER exit sites (dpeaa)DE-He213 membrane trafficking (dpeaa)DE-He213 modelling (dpeaa)DE-He213 photobleaching (dpeaa)DE-He213 Miura, Kota verfasserin aut Weiss, Matthias verfasserin aut Pepperkok, Rainer verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 25(2006), 13 vom: 22. Juni, Seite 2953-2965 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:25 year:2006 number:13 day:22 month:06 pages:2953-2965 https://dx.doi.org/10.1038/sj.emboj.7601205 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_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 25 2006 13 22 06 2953-2965 |
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Runz, Heiko @@aut@@ Miura, Kota @@aut@@ Weiss, Matthias @@aut@@ Pepperkok, Rainer @@aut@@ |
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Runz, Heiko |
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Runz, Heiko misc cholesterol misc ER exit sites misc membrane trafficking misc modelling misc photobleaching Sterols regulate ER‐export dynamics of secretory cargo protein ts‐O45‐G |
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Sterols regulate ER‐export dynamics of secretory cargo protein ts‐O45‐G cholesterol (dpeaa)DE-He213 ER exit sites (dpeaa)DE-He213 membrane trafficking (dpeaa)DE-He213 modelling (dpeaa)DE-He213 photobleaching (dpeaa)DE-He213 |
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misc cholesterol misc ER exit sites misc membrane trafficking misc modelling misc photobleaching |
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Sterols regulate ER‐export dynamics of secretory cargo protein ts‐O45‐G |
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Sterols regulate ER‐export dynamics of secretory cargo protein ts‐O45‐G |
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sterols regulate er‐export dynamics of secretory cargo protein ts‐o45‐g |
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Sterols regulate ER‐export dynamics of secretory cargo protein ts‐O45‐G |
abstract |
Abstract Alterations in endoplasmic reticulum (ER) cholesterol are fundamental for a variety of cellular processes such as the regulation of lipid homeostasis or efficient protein degradation. We show that reduced levels of cellular sterols cause a delayed ER‐to‐Golgi transport of the secretory cargo membrane protein ts‐O45‐G and a relocation to the ER of an endogenous protein cycling between the ER and the Golgi complex. Transport inhibition is characterized by a delay in the accumulation of ts‐O45‐G in ER‐exit sites (ERES) and correlates with a reduced mobility of ts‐O45‐G within ER membranes. A simple mathematical model describing the kinetics of ER‐exit predicts that reduced cargo loading to ERES and not the reduced mobility of ts‐O45‐G accounts for the delayed ER‐exit and arrival at the Golgi. Consistent with this, membrane turnover of the COPII component Sec23p is delayed in sterol‐depleted cells. Altogether, our results demonstrate the importance of sterol levels in COPII mediated ER‐export. © European Molecular Biology Organization 2006 |
abstractGer |
Abstract Alterations in endoplasmic reticulum (ER) cholesterol are fundamental for a variety of cellular processes such as the regulation of lipid homeostasis or efficient protein degradation. We show that reduced levels of cellular sterols cause a delayed ER‐to‐Golgi transport of the secretory cargo membrane protein ts‐O45‐G and a relocation to the ER of an endogenous protein cycling between the ER and the Golgi complex. Transport inhibition is characterized by a delay in the accumulation of ts‐O45‐G in ER‐exit sites (ERES) and correlates with a reduced mobility of ts‐O45‐G within ER membranes. A simple mathematical model describing the kinetics of ER‐exit predicts that reduced cargo loading to ERES and not the reduced mobility of ts‐O45‐G accounts for the delayed ER‐exit and arrival at the Golgi. Consistent with this, membrane turnover of the COPII component Sec23p is delayed in sterol‐depleted cells. Altogether, our results demonstrate the importance of sterol levels in COPII mediated ER‐export. © European Molecular Biology Organization 2006 |
abstract_unstemmed |
Abstract Alterations in endoplasmic reticulum (ER) cholesterol are fundamental for a variety of cellular processes such as the regulation of lipid homeostasis or efficient protein degradation. We show that reduced levels of cellular sterols cause a delayed ER‐to‐Golgi transport of the secretory cargo membrane protein ts‐O45‐G and a relocation to the ER of an endogenous protein cycling between the ER and the Golgi complex. Transport inhibition is characterized by a delay in the accumulation of ts‐O45‐G in ER‐exit sites (ERES) and correlates with a reduced mobility of ts‐O45‐G within ER membranes. A simple mathematical model describing the kinetics of ER‐exit predicts that reduced cargo loading to ERES and not the reduced mobility of ts‐O45‐G accounts for the delayed ER‐exit and arrival at the Golgi. Consistent with this, membrane turnover of the COPII component Sec23p is delayed in sterol‐depleted cells. Altogether, our results demonstrate the importance of sterol levels in COPII mediated ER‐export. © European Molecular Biology Organization 2006 |
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title_short |
Sterols regulate ER‐export dynamics of secretory cargo protein ts‐O45‐G |
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https://dx.doi.org/10.1038/sj.emboj.7601205 |
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Miura, Kota Weiss, Matthias Pepperkok, Rainer |
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score |
7.403063 |