TIP150 interacts with and targets MCAK at the microtubule plus ends
Abstract The microtubule (MT) cytoskeleton orchestrates the cellular plasticity and dynamics that underlie morphogenesis and cell division. Growing MT plus ends have emerged as dynamic regulatory machineries in which specialized proteins—called plus‐end tracking proteins (+TIPs)—bind to and control...
Ausführliche Beschreibung
Autor*in: |
Jiang, Kai [verfasserIn] Wang, Jianyu [verfasserIn] Liu, Jing [verfasserIn] Ward, Tarsha [verfasserIn] Wordeman, Linda [verfasserIn] Davidson, Alec [verfasserIn] Wang, Fengsong [verfasserIn] Yao, Xuebiao [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2009 |
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Anmerkung: |
© European Molecular Biology Organization 2009 |
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Übergeordnetes Werk: |
Enthalten in: EMBO Reports - Nature Publishing Group UK, 2023, 10(2009), 8 vom: 19. Juni, Seite 857-865 |
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Übergeordnetes Werk: |
volume:10 ; year:2009 ; number:8 ; day:19 ; month:06 ; pages:857-865 |
Links: |
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DOI / URN: |
10.1038/embor.2009.94 |
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Katalog-ID: |
SPR058081496 |
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520 | |a Abstract The microtubule (MT) cytoskeleton orchestrates the cellular plasticity and dynamics that underlie morphogenesis and cell division. Growing MT plus ends have emerged as dynamic regulatory machineries in which specialized proteins—called plus‐end tracking proteins (+TIPs)—bind to and control the plus‐end dynamics that are essential for cell division and migration. However, the molecular mechanisms underlying the plus‐end regulation by +TIPs at spindle and astral MTs have remained elusive. Here, we show that TIP150 is a new +TIP that binds to end‐binding protein 1 (EB1) in vitro and co‐localizes with EB1 at the MT plus ends in vivo. Suppression of EB1 eliminates the plus‐end localization of TIP150. Interestingly, TIP150 also binds to mitotic centromere‐associated kinesin (MCAK), an MT depolymerase that localizes to the plus end of MTs. Suppression of TIP150 diminishes the plus‐end localization of MCAK. Importantly, aurora B‐mediated phosphorylation disrupts the TIP150–MCAK association in vitro. We reason that TIP150 facilitates the EB1‐dependent loading of MCAK onto MT plus ends and orchestrates the dynamics at the plus end of MTs. | ||
650 | 4 | |a microtubule |7 (dpeaa)DE-He213 | |
650 | 4 | |a MAP |7 (dpeaa)DE-He213 | |
650 | 4 | |a TIP150 |7 (dpeaa)DE-He213 | |
650 | 4 | |a MCAK |7 (dpeaa)DE-He213 | |
650 | 4 | |a EB1 |7 (dpeaa)DE-He213 | |
700 | 1 | |a Wang, Jianyu |e verfasserin |4 aut | |
700 | 1 | |a Liu, Jing |e verfasserin |4 aut | |
700 | 1 | |a Ward, Tarsha |e verfasserin |4 aut | |
700 | 1 | |a Wordeman, Linda |e verfasserin |4 aut | |
700 | 1 | |a Davidson, Alec |e verfasserin |4 aut | |
700 | 1 | |a Wang, Fengsong |e verfasserin |4 aut | |
700 | 1 | |a Yao, Xuebiao |e verfasserin |4 aut | |
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10.1038/embor.2009.94 doi (DE-627)SPR058081496 (SPR)embor.2009.94-e DE-627 ger DE-627 rakwb eng Jiang, Kai verfasserin aut TIP150 interacts with and targets MCAK at the microtubule plus ends 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2009 Abstract The microtubule (MT) cytoskeleton orchestrates the cellular plasticity and dynamics that underlie morphogenesis and cell division. Growing MT plus ends have emerged as dynamic regulatory machineries in which specialized proteins—called plus‐end tracking proteins (+TIPs)—bind to and control the plus‐end dynamics that are essential for cell division and migration. However, the molecular mechanisms underlying the plus‐end regulation by +TIPs at spindle and astral MTs have remained elusive. Here, we show that TIP150 is a new +TIP that binds to end‐binding protein 1 (EB1) in vitro and co‐localizes with EB1 at the MT plus ends in vivo. Suppression of EB1 eliminates the plus‐end localization of TIP150. Interestingly, TIP150 also binds to mitotic centromere‐associated kinesin (MCAK), an MT depolymerase that localizes to the plus end of MTs. Suppression of TIP150 diminishes the plus‐end localization of MCAK. Importantly, aurora B‐mediated phosphorylation disrupts the TIP150–MCAK association in vitro. We reason that TIP150 facilitates the EB1‐dependent loading of MCAK onto MT plus ends and orchestrates the dynamics at the plus end of MTs. microtubule (dpeaa)DE-He213 MAP (dpeaa)DE-He213 TIP150 (dpeaa)DE-He213 MCAK (dpeaa)DE-He213 EB1 (dpeaa)DE-He213 Wang, Jianyu verfasserin aut Liu, Jing verfasserin aut Ward, Tarsha verfasserin aut Wordeman, Linda verfasserin aut Davidson, Alec verfasserin aut Wang, Fengsong verfasserin aut Yao, Xuebiao verfasserin aut Enthalten in EMBO Reports Nature Publishing Group UK, 2023 10(2009), 8 vom: 19. Juni, Seite 857-865 (DE-627)320645622 (DE-600)2025376-X 1469-3178 nnns volume:10 year:2009 number:8 day:19 month:06 pages:857-865 https://dx.doi.org/10.1038/embor.2009.94 X:SPRINGER Resolving-System kostenfrei 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 10 2009 8 19 06 857-865 |
spelling |
10.1038/embor.2009.94 doi (DE-627)SPR058081496 (SPR)embor.2009.94-e DE-627 ger DE-627 rakwb eng Jiang, Kai verfasserin aut TIP150 interacts with and targets MCAK at the microtubule plus ends 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2009 Abstract The microtubule (MT) cytoskeleton orchestrates the cellular plasticity and dynamics that underlie morphogenesis and cell division. Growing MT plus ends have emerged as dynamic regulatory machineries in which specialized proteins—called plus‐end tracking proteins (+TIPs)—bind to and control the plus‐end dynamics that are essential for cell division and migration. However, the molecular mechanisms underlying the plus‐end regulation by +TIPs at spindle and astral MTs have remained elusive. Here, we show that TIP150 is a new +TIP that binds to end‐binding protein 1 (EB1) in vitro and co‐localizes with EB1 at the MT plus ends in vivo. Suppression of EB1 eliminates the plus‐end localization of TIP150. Interestingly, TIP150 also binds to mitotic centromere‐associated kinesin (MCAK), an MT depolymerase that localizes to the plus end of MTs. Suppression of TIP150 diminishes the plus‐end localization of MCAK. Importantly, aurora B‐mediated phosphorylation disrupts the TIP150–MCAK association in vitro. We reason that TIP150 facilitates the EB1‐dependent loading of MCAK onto MT plus ends and orchestrates the dynamics at the plus end of MTs. microtubule (dpeaa)DE-He213 MAP (dpeaa)DE-He213 TIP150 (dpeaa)DE-He213 MCAK (dpeaa)DE-He213 EB1 (dpeaa)DE-He213 Wang, Jianyu verfasserin aut Liu, Jing verfasserin aut Ward, Tarsha verfasserin aut Wordeman, Linda verfasserin aut Davidson, Alec verfasserin aut Wang, Fengsong verfasserin aut Yao, Xuebiao verfasserin aut Enthalten in EMBO Reports Nature Publishing Group UK, 2023 10(2009), 8 vom: 19. Juni, Seite 857-865 (DE-627)320645622 (DE-600)2025376-X 1469-3178 nnns volume:10 year:2009 number:8 day:19 month:06 pages:857-865 https://dx.doi.org/10.1038/embor.2009.94 X:SPRINGER Resolving-System kostenfrei 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 10 2009 8 19 06 857-865 |
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10.1038/embor.2009.94 doi (DE-627)SPR058081496 (SPR)embor.2009.94-e DE-627 ger DE-627 rakwb eng Jiang, Kai verfasserin aut TIP150 interacts with and targets MCAK at the microtubule plus ends 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2009 Abstract The microtubule (MT) cytoskeleton orchestrates the cellular plasticity and dynamics that underlie morphogenesis and cell division. Growing MT plus ends have emerged as dynamic regulatory machineries in which specialized proteins—called plus‐end tracking proteins (+TIPs)—bind to and control the plus‐end dynamics that are essential for cell division and migration. However, the molecular mechanisms underlying the plus‐end regulation by +TIPs at spindle and astral MTs have remained elusive. Here, we show that TIP150 is a new +TIP that binds to end‐binding protein 1 (EB1) in vitro and co‐localizes with EB1 at the MT plus ends in vivo. Suppression of EB1 eliminates the plus‐end localization of TIP150. Interestingly, TIP150 also binds to mitotic centromere‐associated kinesin (MCAK), an MT depolymerase that localizes to the plus end of MTs. Suppression of TIP150 diminishes the plus‐end localization of MCAK. Importantly, aurora B‐mediated phosphorylation disrupts the TIP150–MCAK association in vitro. We reason that TIP150 facilitates the EB1‐dependent loading of MCAK onto MT plus ends and orchestrates the dynamics at the plus end of MTs. microtubule (dpeaa)DE-He213 MAP (dpeaa)DE-He213 TIP150 (dpeaa)DE-He213 MCAK (dpeaa)DE-He213 EB1 (dpeaa)DE-He213 Wang, Jianyu verfasserin aut Liu, Jing verfasserin aut Ward, Tarsha verfasserin aut Wordeman, Linda verfasserin aut Davidson, Alec verfasserin aut Wang, Fengsong verfasserin aut Yao, Xuebiao verfasserin aut Enthalten in EMBO Reports Nature Publishing Group UK, 2023 10(2009), 8 vom: 19. Juni, Seite 857-865 (DE-627)320645622 (DE-600)2025376-X 1469-3178 nnns volume:10 year:2009 number:8 day:19 month:06 pages:857-865 https://dx.doi.org/10.1038/embor.2009.94 X:SPRINGER Resolving-System kostenfrei 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 10 2009 8 19 06 857-865 |
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10.1038/embor.2009.94 doi (DE-627)SPR058081496 (SPR)embor.2009.94-e DE-627 ger DE-627 rakwb eng Jiang, Kai verfasserin aut TIP150 interacts with and targets MCAK at the microtubule plus ends 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2009 Abstract The microtubule (MT) cytoskeleton orchestrates the cellular plasticity and dynamics that underlie morphogenesis and cell division. Growing MT plus ends have emerged as dynamic regulatory machineries in which specialized proteins—called plus‐end tracking proteins (+TIPs)—bind to and control the plus‐end dynamics that are essential for cell division and migration. However, the molecular mechanisms underlying the plus‐end regulation by +TIPs at spindle and astral MTs have remained elusive. Here, we show that TIP150 is a new +TIP that binds to end‐binding protein 1 (EB1) in vitro and co‐localizes with EB1 at the MT plus ends in vivo. Suppression of EB1 eliminates the plus‐end localization of TIP150. Interestingly, TIP150 also binds to mitotic centromere‐associated kinesin (MCAK), an MT depolymerase that localizes to the plus end of MTs. Suppression of TIP150 diminishes the plus‐end localization of MCAK. Importantly, aurora B‐mediated phosphorylation disrupts the TIP150–MCAK association in vitro. We reason that TIP150 facilitates the EB1‐dependent loading of MCAK onto MT plus ends and orchestrates the dynamics at the plus end of MTs. microtubule (dpeaa)DE-He213 MAP (dpeaa)DE-He213 TIP150 (dpeaa)DE-He213 MCAK (dpeaa)DE-He213 EB1 (dpeaa)DE-He213 Wang, Jianyu verfasserin aut Liu, Jing verfasserin aut Ward, Tarsha verfasserin aut Wordeman, Linda verfasserin aut Davidson, Alec verfasserin aut Wang, Fengsong verfasserin aut Yao, Xuebiao verfasserin aut Enthalten in EMBO Reports Nature Publishing Group UK, 2023 10(2009), 8 vom: 19. Juni, Seite 857-865 (DE-627)320645622 (DE-600)2025376-X 1469-3178 nnns volume:10 year:2009 number:8 day:19 month:06 pages:857-865 https://dx.doi.org/10.1038/embor.2009.94 X:SPRINGER Resolving-System kostenfrei 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 10 2009 8 19 06 857-865 |
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10.1038/embor.2009.94 doi (DE-627)SPR058081496 (SPR)embor.2009.94-e DE-627 ger DE-627 rakwb eng Jiang, Kai verfasserin aut TIP150 interacts with and targets MCAK at the microtubule plus ends 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2009 Abstract The microtubule (MT) cytoskeleton orchestrates the cellular plasticity and dynamics that underlie morphogenesis and cell division. Growing MT plus ends have emerged as dynamic regulatory machineries in which specialized proteins—called plus‐end tracking proteins (+TIPs)—bind to and control the plus‐end dynamics that are essential for cell division and migration. However, the molecular mechanisms underlying the plus‐end regulation by +TIPs at spindle and astral MTs have remained elusive. Here, we show that TIP150 is a new +TIP that binds to end‐binding protein 1 (EB1) in vitro and co‐localizes with EB1 at the MT plus ends in vivo. Suppression of EB1 eliminates the plus‐end localization of TIP150. Interestingly, TIP150 also binds to mitotic centromere‐associated kinesin (MCAK), an MT depolymerase that localizes to the plus end of MTs. Suppression of TIP150 diminishes the plus‐end localization of MCAK. Importantly, aurora B‐mediated phosphorylation disrupts the TIP150–MCAK association in vitro. We reason that TIP150 facilitates the EB1‐dependent loading of MCAK onto MT plus ends and orchestrates the dynamics at the plus end of MTs. microtubule (dpeaa)DE-He213 MAP (dpeaa)DE-He213 TIP150 (dpeaa)DE-He213 MCAK (dpeaa)DE-He213 EB1 (dpeaa)DE-He213 Wang, Jianyu verfasserin aut Liu, Jing verfasserin aut Ward, Tarsha verfasserin aut Wordeman, Linda verfasserin aut Davidson, Alec verfasserin aut Wang, Fengsong verfasserin aut Yao, Xuebiao verfasserin aut Enthalten in EMBO Reports Nature Publishing Group UK, 2023 10(2009), 8 vom: 19. Juni, Seite 857-865 (DE-627)320645622 (DE-600)2025376-X 1469-3178 nnns volume:10 year:2009 number:8 day:19 month:06 pages:857-865 https://dx.doi.org/10.1038/embor.2009.94 X:SPRINGER Resolving-System kostenfrei 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 10 2009 8 19 06 857-865 |
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Jiang, Kai @@aut@@ Wang, Jianyu @@aut@@ Liu, Jing @@aut@@ Ward, Tarsha @@aut@@ Wordeman, Linda @@aut@@ Davidson, Alec @@aut@@ Wang, Fengsong @@aut@@ Yao, Xuebiao @@aut@@ |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000naa a22002652 4500</leader><controlfield tag="001">SPR058081496</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20241025065137.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">241025s2009 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1038/embor.2009.94</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR058081496</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)embor.2009.94-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Jiang, Kai</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">TIP150 interacts with and targets MCAK at the microtubule plus ends</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2009</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© European Molecular Biology Organization 2009</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract The microtubule (MT) cytoskeleton orchestrates the cellular plasticity and dynamics that underlie morphogenesis and cell division. Growing MT plus ends have emerged as dynamic regulatory machineries in which specialized proteins—called plus‐end tracking proteins (+TIPs)—bind to and control the plus‐end dynamics that are essential for cell division and migration. However, the molecular mechanisms underlying the plus‐end regulation by +TIPs at spindle and astral MTs have remained elusive. Here, we show that TIP150 is a new +TIP that binds to end‐binding protein 1 (EB1) in vitro and co‐localizes with EB1 at the MT plus ends in vivo. Suppression of EB1 eliminates the plus‐end localization of TIP150. Interestingly, TIP150 also binds to mitotic centromere‐associated kinesin (MCAK), an MT depolymerase that localizes to the plus end of MTs. Suppression of TIP150 diminishes the plus‐end localization of MCAK. Importantly, aurora B‐mediated phosphorylation disrupts the TIP150–MCAK association in vitro. 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|
author |
Jiang, Kai |
spellingShingle |
Jiang, Kai misc microtubule misc MAP misc TIP150 misc MCAK misc EB1 TIP150 interacts with and targets MCAK at the microtubule plus ends |
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Jiang, Kai |
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1469-3178 |
topic_title |
TIP150 interacts with and targets MCAK at the microtubule plus ends microtubule (dpeaa)DE-He213 MAP (dpeaa)DE-He213 TIP150 (dpeaa)DE-He213 MCAK (dpeaa)DE-He213 EB1 (dpeaa)DE-He213 |
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misc microtubule misc MAP misc TIP150 misc MCAK misc EB1 |
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misc microtubule misc MAP misc TIP150 misc MCAK misc EB1 |
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misc microtubule misc MAP misc TIP150 misc MCAK misc EB1 |
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Elektronische Aufsätze Aufsätze Elektronische Ressource |
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TIP150 interacts with and targets MCAK at the microtubule plus ends |
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TIP150 interacts with and targets MCAK at the microtubule plus ends |
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Jiang, Kai |
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Jiang, Kai Wang, Jianyu Liu, Jing Ward, Tarsha Wordeman, Linda Davidson, Alec Wang, Fengsong Yao, Xuebiao |
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Elektronische Aufsätze |
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tip150 interacts with and targets mcak at the microtubule plus ends |
title_auth |
TIP150 interacts with and targets MCAK at the microtubule plus ends |
abstract |
Abstract The microtubule (MT) cytoskeleton orchestrates the cellular plasticity and dynamics that underlie morphogenesis and cell division. Growing MT plus ends have emerged as dynamic regulatory machineries in which specialized proteins—called plus‐end tracking proteins (+TIPs)—bind to and control the plus‐end dynamics that are essential for cell division and migration. However, the molecular mechanisms underlying the plus‐end regulation by +TIPs at spindle and astral MTs have remained elusive. Here, we show that TIP150 is a new +TIP that binds to end‐binding protein 1 (EB1) in vitro and co‐localizes with EB1 at the MT plus ends in vivo. Suppression of EB1 eliminates the plus‐end localization of TIP150. Interestingly, TIP150 also binds to mitotic centromere‐associated kinesin (MCAK), an MT depolymerase that localizes to the plus end of MTs. Suppression of TIP150 diminishes the plus‐end localization of MCAK. Importantly, aurora B‐mediated phosphorylation disrupts the TIP150–MCAK association in vitro. We reason that TIP150 facilitates the EB1‐dependent loading of MCAK onto MT plus ends and orchestrates the dynamics at the plus end of MTs. © European Molecular Biology Organization 2009 |
abstractGer |
Abstract The microtubule (MT) cytoskeleton orchestrates the cellular plasticity and dynamics that underlie morphogenesis and cell division. Growing MT plus ends have emerged as dynamic regulatory machineries in which specialized proteins—called plus‐end tracking proteins (+TIPs)—bind to and control the plus‐end dynamics that are essential for cell division and migration. However, the molecular mechanisms underlying the plus‐end regulation by +TIPs at spindle and astral MTs have remained elusive. Here, we show that TIP150 is a new +TIP that binds to end‐binding protein 1 (EB1) in vitro and co‐localizes with EB1 at the MT plus ends in vivo. Suppression of EB1 eliminates the plus‐end localization of TIP150. Interestingly, TIP150 also binds to mitotic centromere‐associated kinesin (MCAK), an MT depolymerase that localizes to the plus end of MTs. Suppression of TIP150 diminishes the plus‐end localization of MCAK. Importantly, aurora B‐mediated phosphorylation disrupts the TIP150–MCAK association in vitro. We reason that TIP150 facilitates the EB1‐dependent loading of MCAK onto MT plus ends and orchestrates the dynamics at the plus end of MTs. © European Molecular Biology Organization 2009 |
abstract_unstemmed |
Abstract The microtubule (MT) cytoskeleton orchestrates the cellular plasticity and dynamics that underlie morphogenesis and cell division. Growing MT plus ends have emerged as dynamic regulatory machineries in which specialized proteins—called plus‐end tracking proteins (+TIPs)—bind to and control the plus‐end dynamics that are essential for cell division and migration. However, the molecular mechanisms underlying the plus‐end regulation by +TIPs at spindle and astral MTs have remained elusive. Here, we show that TIP150 is a new +TIP that binds to end‐binding protein 1 (EB1) in vitro and co‐localizes with EB1 at the MT plus ends in vivo. Suppression of EB1 eliminates the plus‐end localization of TIP150. Interestingly, TIP150 also binds to mitotic centromere‐associated kinesin (MCAK), an MT depolymerase that localizes to the plus end of MTs. Suppression of TIP150 diminishes the plus‐end localization of MCAK. Importantly, aurora B‐mediated phosphorylation disrupts the TIP150–MCAK association in vitro. We reason that TIP150 facilitates the EB1‐dependent loading of MCAK onto MT plus ends and orchestrates the dynamics at the plus end of MTs. © European Molecular Biology Organization 2009 |
collection_details |
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container_issue |
8 |
title_short |
TIP150 interacts with and targets MCAK at the microtubule plus ends |
url |
https://dx.doi.org/10.1038/embor.2009.94 |
remote_bool |
true |
author2 |
Wang, Jianyu Liu, Jing Ward, Tarsha Wordeman, Linda Davidson, Alec Wang, Fengsong Yao, Xuebiao |
author2Str |
Wang, Jianyu Liu, Jing Ward, Tarsha Wordeman, Linda Davidson, Alec Wang, Fengsong Yao, Xuebiao |
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hochschulschrift_bool |
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doi_str |
10.1038/embor.2009.94 |
up_date |
2024-10-25T04:56:19.485Z |
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|
score |
7.4011765 |