Tau phosphorylation regulates the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain

Introduction The application of high-throughput genomic approaches has revealed 24 novel risk loci for Alzheimer’s disease (AD). We recently reported that the bridging integrator 1 (BIN1) risk gene is linked to Tau pathology. Results We used glutathione S-transferase pull-down assays and nuclear mag...
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Autor*in:	Sottejeau, Yoann [verfasserIn] Bretteville, Alexis Cantrelle, François-Xavier Malmanche, Nicolas Demiaute, Florie Mendes, Tiago Delay, Charlotte Alves Dos Alves, Harmony Flaig, Amandine Davies, Peter Dourlen, Pierre Dermaut, Bart Laporte, Jocelyn Amouyel, Philippe Lippens, Guy Chapuis, Julien Landrieu, Isabelle Lambert, Jean-Charles

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2015

Schlagwörter:	Nuclear Magnetic Resonance Primary Neuron Nuclear Magnetic Resonance Experiment Primary Neuron Culture Heteronuclear Single Quantum Coherence

Anmerkung:	© Sottejeau et al. 2015

Übergeordnetes Werk:	Enthalten in: Acta Neuropathologica Communications - London : Biomed Central, 2013, 3(2015), 1 vom: 23. Sept.
Übergeordnetes Werk:	volume:3 ; year:2015 ; number:1 ; day:23 ; month:09

Links:	Volltext

DOI / URN:	10.1186/s40478-015-0237-8

Katalog-ID:	SPR036509892

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allfields	10.1186/s40478-015-0237-8 doi (DE-627)SPR036509892 (SPR)s40478-015-0237-8-e DE-627 ger DE-627 rakwb eng Sottejeau, Yoann verfasserin aut Tau phosphorylation regulates the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Sottejeau et al. 2015 Introduction The application of high-throughput genomic approaches has revealed 24 novel risk loci for Alzheimer’s disease (AD). We recently reported that the bridging integrator 1 (BIN1) risk gene is linked to Tau pathology. Results We used glutathione S-transferase pull-down assays and nuclear magnetic resonance (NMR) experiments to demonstrate that BIN1 and Tau proteins interact directly and then map the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain (PRD) . Our NMR data showed that Tau phosphorylation at Thr231 weakens the SH3-PRD interaction. Using primary neurons, we found that BIN1-Tau complexes partly co-localize with the actin cytoskeleton; however, these complexes were not observed with Thr231-phosphorylated Tau species. Conclusion Our results show that (i) BIN1 and Tau bind through an SH3-PRD interaction and (ii) the interaction is downregulated by phosphorylation of Tau Thr231 (and potentially other residues). Our study sheds new light on regulation of the BIN1/Tau interaction and opens up new avenues for exploring its complex’s role in the pathogenesis of AD. Nuclear Magnetic Resonance (dpeaa)DE-He213 Primary Neuron (dpeaa)DE-He213 Nuclear Magnetic Resonance Experiment (dpeaa)DE-He213 Primary Neuron Culture (dpeaa)DE-He213 Heteronuclear Single Quantum Coherence (dpeaa)DE-He213 Bretteville, Alexis aut Cantrelle, François-Xavier aut Malmanche, Nicolas aut Demiaute, Florie aut Mendes, Tiago aut Delay, Charlotte aut Alves Dos Alves, Harmony aut Flaig, Amandine aut Davies, Peter aut Dourlen, Pierre aut Dermaut, Bart aut Laporte, Jocelyn aut Amouyel, Philippe aut Lippens, Guy aut Chapuis, Julien aut Landrieu, Isabelle aut Lambert, Jean-Charles aut Enthalten in Acta Neuropathologica Communications London : Biomed Central, 2013 3(2015), 1 vom: 23. Sept. (DE-627)746066465 (DE-600)2715589-4 2051-5960 nnns volume:3 year:2015 number:1 day:23 month:09 https://dx.doi.org/10.1186/s40478-015-0237-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2015 1 23 09
spelling	10.1186/s40478-015-0237-8 doi (DE-627)SPR036509892 (SPR)s40478-015-0237-8-e DE-627 ger DE-627 rakwb eng Sottejeau, Yoann verfasserin aut Tau phosphorylation regulates the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Sottejeau et al. 2015 Introduction The application of high-throughput genomic approaches has revealed 24 novel risk loci for Alzheimer’s disease (AD). We recently reported that the bridging integrator 1 (BIN1) risk gene is linked to Tau pathology. Results We used glutathione S-transferase pull-down assays and nuclear magnetic resonance (NMR) experiments to demonstrate that BIN1 and Tau proteins interact directly and then map the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain (PRD) . Our NMR data showed that Tau phosphorylation at Thr231 weakens the SH3-PRD interaction. Using primary neurons, we found that BIN1-Tau complexes partly co-localize with the actin cytoskeleton; however, these complexes were not observed with Thr231-phosphorylated Tau species. Conclusion Our results show that (i) BIN1 and Tau bind through an SH3-PRD interaction and (ii) the interaction is downregulated by phosphorylation of Tau Thr231 (and potentially other residues). Our study sheds new light on regulation of the BIN1/Tau interaction and opens up new avenues for exploring its complex’s role in the pathogenesis of AD. Nuclear Magnetic Resonance (dpeaa)DE-He213 Primary Neuron (dpeaa)DE-He213 Nuclear Magnetic Resonance Experiment (dpeaa)DE-He213 Primary Neuron Culture (dpeaa)DE-He213 Heteronuclear Single Quantum Coherence (dpeaa)DE-He213 Bretteville, Alexis aut Cantrelle, François-Xavier aut Malmanche, Nicolas aut Demiaute, Florie aut Mendes, Tiago aut Delay, Charlotte aut Alves Dos Alves, Harmony aut Flaig, Amandine aut Davies, Peter aut Dourlen, Pierre aut Dermaut, Bart aut Laporte, Jocelyn aut Amouyel, Philippe aut Lippens, Guy aut Chapuis, Julien aut Landrieu, Isabelle aut Lambert, Jean-Charles aut Enthalten in Acta Neuropathologica Communications London : Biomed Central, 2013 3(2015), 1 vom: 23. Sept. (DE-627)746066465 (DE-600)2715589-4 2051-5960 nnns volume:3 year:2015 number:1 day:23 month:09 https://dx.doi.org/10.1186/s40478-015-0237-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2015 1 23 09
allfields_unstemmed	10.1186/s40478-015-0237-8 doi (DE-627)SPR036509892 (SPR)s40478-015-0237-8-e DE-627 ger DE-627 rakwb eng Sottejeau, Yoann verfasserin aut Tau phosphorylation regulates the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Sottejeau et al. 2015 Introduction The application of high-throughput genomic approaches has revealed 24 novel risk loci for Alzheimer’s disease (AD). We recently reported that the bridging integrator 1 (BIN1) risk gene is linked to Tau pathology. Results We used glutathione S-transferase pull-down assays and nuclear magnetic resonance (NMR) experiments to demonstrate that BIN1 and Tau proteins interact directly and then map the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain (PRD) . Our NMR data showed that Tau phosphorylation at Thr231 weakens the SH3-PRD interaction. Using primary neurons, we found that BIN1-Tau complexes partly co-localize with the actin cytoskeleton; however, these complexes were not observed with Thr231-phosphorylated Tau species. Conclusion Our results show that (i) BIN1 and Tau bind through an SH3-PRD interaction and (ii) the interaction is downregulated by phosphorylation of Tau Thr231 (and potentially other residues). Our study sheds new light on regulation of the BIN1/Tau interaction and opens up new avenues for exploring its complex’s role in the pathogenesis of AD. Nuclear Magnetic Resonance (dpeaa)DE-He213 Primary Neuron (dpeaa)DE-He213 Nuclear Magnetic Resonance Experiment (dpeaa)DE-He213 Primary Neuron Culture (dpeaa)DE-He213 Heteronuclear Single Quantum Coherence (dpeaa)DE-He213 Bretteville, Alexis aut Cantrelle, François-Xavier aut Malmanche, Nicolas aut Demiaute, Florie aut Mendes, Tiago aut Delay, Charlotte aut Alves Dos Alves, Harmony aut Flaig, Amandine aut Davies, Peter aut Dourlen, Pierre aut Dermaut, Bart aut Laporte, Jocelyn aut Amouyel, Philippe aut Lippens, Guy aut Chapuis, Julien aut Landrieu, Isabelle aut Lambert, Jean-Charles aut Enthalten in Acta Neuropathologica Communications London : Biomed Central, 2013 3(2015), 1 vom: 23. Sept. (DE-627)746066465 (DE-600)2715589-4 2051-5960 nnns volume:3 year:2015 number:1 day:23 month:09 https://dx.doi.org/10.1186/s40478-015-0237-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2015 1 23 09
allfieldsGer	10.1186/s40478-015-0237-8 doi (DE-627)SPR036509892 (SPR)s40478-015-0237-8-e DE-627 ger DE-627 rakwb eng Sottejeau, Yoann verfasserin aut Tau phosphorylation regulates the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Sottejeau et al. 2015 Introduction The application of high-throughput genomic approaches has revealed 24 novel risk loci for Alzheimer’s disease (AD). We recently reported that the bridging integrator 1 (BIN1) risk gene is linked to Tau pathology. Results We used glutathione S-transferase pull-down assays and nuclear magnetic resonance (NMR) experiments to demonstrate that BIN1 and Tau proteins interact directly and then map the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain (PRD) . Our NMR data showed that Tau phosphorylation at Thr231 weakens the SH3-PRD interaction. Using primary neurons, we found that BIN1-Tau complexes partly co-localize with the actin cytoskeleton; however, these complexes were not observed with Thr231-phosphorylated Tau species. Conclusion Our results show that (i) BIN1 and Tau bind through an SH3-PRD interaction and (ii) the interaction is downregulated by phosphorylation of Tau Thr231 (and potentially other residues). Our study sheds new light on regulation of the BIN1/Tau interaction and opens up new avenues for exploring its complex’s role in the pathogenesis of AD. Nuclear Magnetic Resonance (dpeaa)DE-He213 Primary Neuron (dpeaa)DE-He213 Nuclear Magnetic Resonance Experiment (dpeaa)DE-He213 Primary Neuron Culture (dpeaa)DE-He213 Heteronuclear Single Quantum Coherence (dpeaa)DE-He213 Bretteville, Alexis aut Cantrelle, François-Xavier aut Malmanche, Nicolas aut Demiaute, Florie aut Mendes, Tiago aut Delay, Charlotte aut Alves Dos Alves, Harmony aut Flaig, Amandine aut Davies, Peter aut Dourlen, Pierre aut Dermaut, Bart aut Laporte, Jocelyn aut Amouyel, Philippe aut Lippens, Guy aut Chapuis, Julien aut Landrieu, Isabelle aut Lambert, Jean-Charles aut Enthalten in Acta Neuropathologica Communications London : Biomed Central, 2013 3(2015), 1 vom: 23. Sept. (DE-627)746066465 (DE-600)2715589-4 2051-5960 nnns volume:3 year:2015 number:1 day:23 month:09 https://dx.doi.org/10.1186/s40478-015-0237-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2015 1 23 09
allfieldsSound	10.1186/s40478-015-0237-8 doi (DE-627)SPR036509892 (SPR)s40478-015-0237-8-e DE-627 ger DE-627 rakwb eng Sottejeau, Yoann verfasserin aut Tau phosphorylation regulates the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Sottejeau et al. 2015 Introduction The application of high-throughput genomic approaches has revealed 24 novel risk loci for Alzheimer’s disease (AD). We recently reported that the bridging integrator 1 (BIN1) risk gene is linked to Tau pathology. Results We used glutathione S-transferase pull-down assays and nuclear magnetic resonance (NMR) experiments to demonstrate that BIN1 and Tau proteins interact directly and then map the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain (PRD) . Our NMR data showed that Tau phosphorylation at Thr231 weakens the SH3-PRD interaction. Using primary neurons, we found that BIN1-Tau complexes partly co-localize with the actin cytoskeleton; however, these complexes were not observed with Thr231-phosphorylated Tau species. Conclusion Our results show that (i) BIN1 and Tau bind through an SH3-PRD interaction and (ii) the interaction is downregulated by phosphorylation of Tau Thr231 (and potentially other residues). Our study sheds new light on regulation of the BIN1/Tau interaction and opens up new avenues for exploring its complex’s role in the pathogenesis of AD. Nuclear Magnetic Resonance (dpeaa)DE-He213 Primary Neuron (dpeaa)DE-He213 Nuclear Magnetic Resonance Experiment (dpeaa)DE-He213 Primary Neuron Culture (dpeaa)DE-He213 Heteronuclear Single Quantum Coherence (dpeaa)DE-He213 Bretteville, Alexis aut Cantrelle, François-Xavier aut Malmanche, Nicolas aut Demiaute, Florie aut Mendes, Tiago aut Delay, Charlotte aut Alves Dos Alves, Harmony aut Flaig, Amandine aut Davies, Peter aut Dourlen, Pierre aut Dermaut, Bart aut Laporte, Jocelyn aut Amouyel, Philippe aut Lippens, Guy aut Chapuis, Julien aut Landrieu, Isabelle aut Lambert, Jean-Charles aut Enthalten in Acta Neuropathologica Communications London : Biomed Central, 2013 3(2015), 1 vom: 23. Sept. (DE-627)746066465 (DE-600)2715589-4 2051-5960 nnns volume:3 year:2015 number:1 day:23 month:09 https://dx.doi.org/10.1186/s40478-015-0237-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2015 1 23 09
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source	Enthalten in Acta Neuropathologica Communications 3(2015), 1 vom: 23. Sept. volume:3 year:2015 number:1 day:23 month:09
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authorswithroles_txt_mv	Sottejeau, Yoann @@aut@@ Bretteville, Alexis @@aut@@ Cantrelle, François-Xavier @@aut@@ Malmanche, Nicolas @@aut@@ Demiaute, Florie @@aut@@ Mendes, Tiago @@aut@@ Delay, Charlotte @@aut@@ Alves Dos Alves, Harmony @@aut@@ Flaig, Amandine @@aut@@ Davies, Peter @@aut@@ Dourlen, Pierre @@aut@@ Dermaut, Bart @@aut@@ Laporte, Jocelyn @@aut@@ Amouyel, Philippe @@aut@@ Lippens, Guy @@aut@@ Chapuis, Julien @@aut@@ Landrieu, Isabelle @@aut@@ Lambert, Jean-Charles @@aut@@
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author	Sottejeau, Yoann
spellingShingle	Sottejeau, Yoann misc Nuclear Magnetic Resonance misc Primary Neuron misc Nuclear Magnetic Resonance Experiment misc Primary Neuron Culture misc Heteronuclear Single Quantum Coherence Tau phosphorylation regulates the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain
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topic_title	Tau phosphorylation regulates the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain Nuclear Magnetic Resonance (dpeaa)DE-He213 Primary Neuron (dpeaa)DE-He213 Nuclear Magnetic Resonance Experiment (dpeaa)DE-He213 Primary Neuron Culture (dpeaa)DE-He213 Heteronuclear Single Quantum Coherence (dpeaa)DE-He213
topic	misc Nuclear Magnetic Resonance misc Primary Neuron misc Nuclear Magnetic Resonance Experiment misc Primary Neuron Culture misc Heteronuclear Single Quantum Coherence
topic_unstemmed	misc Nuclear Magnetic Resonance misc Primary Neuron misc Nuclear Magnetic Resonance Experiment misc Primary Neuron Culture misc Heteronuclear Single Quantum Coherence
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title	Tau phosphorylation regulates the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain
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title_full	Tau phosphorylation regulates the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain
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author_browse	Sottejeau, Yoann Bretteville, Alexis Cantrelle, François-Xavier Malmanche, Nicolas Demiaute, Florie Mendes, Tiago Delay, Charlotte Alves Dos Alves, Harmony Flaig, Amandine Davies, Peter Dourlen, Pierre Dermaut, Bart Laporte, Jocelyn Amouyel, Philippe Lippens, Guy Chapuis, Julien Landrieu, Isabelle Lambert, Jean-Charles
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title_sort	tau phosphorylation regulates the interaction between bin1’s sh3 domain and tau’s proline-rich domain
title_auth	Tau phosphorylation regulates the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain
abstract	Introduction The application of high-throughput genomic approaches has revealed 24 novel risk loci for Alzheimer’s disease (AD). We recently reported that the bridging integrator 1 (BIN1) risk gene is linked to Tau pathology. Results We used glutathione S-transferase pull-down assays and nuclear magnetic resonance (NMR) experiments to demonstrate that BIN1 and Tau proteins interact directly and then map the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain (PRD) . Our NMR data showed that Tau phosphorylation at Thr231 weakens the SH3-PRD interaction. Using primary neurons, we found that BIN1-Tau complexes partly co-localize with the actin cytoskeleton; however, these complexes were not observed with Thr231-phosphorylated Tau species. Conclusion Our results show that (i) BIN1 and Tau bind through an SH3-PRD interaction and (ii) the interaction is downregulated by phosphorylation of Tau Thr231 (and potentially other residues). Our study sheds new light on regulation of the BIN1/Tau interaction and opens up new avenues for exploring its complex’s role in the pathogenesis of AD. © Sottejeau et al. 2015
abstractGer	Introduction The application of high-throughput genomic approaches has revealed 24 novel risk loci for Alzheimer’s disease (AD). We recently reported that the bridging integrator 1 (BIN1) risk gene is linked to Tau pathology. Results We used glutathione S-transferase pull-down assays and nuclear magnetic resonance (NMR) experiments to demonstrate that BIN1 and Tau proteins interact directly and then map the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain (PRD) . Our NMR data showed that Tau phosphorylation at Thr231 weakens the SH3-PRD interaction. Using primary neurons, we found that BIN1-Tau complexes partly co-localize with the actin cytoskeleton; however, these complexes were not observed with Thr231-phosphorylated Tau species. Conclusion Our results show that (i) BIN1 and Tau bind through an SH3-PRD interaction and (ii) the interaction is downregulated by phosphorylation of Tau Thr231 (and potentially other residues). Our study sheds new light on regulation of the BIN1/Tau interaction and opens up new avenues for exploring its complex’s role in the pathogenesis of AD. © Sottejeau et al. 2015
abstract_unstemmed	Introduction The application of high-throughput genomic approaches has revealed 24 novel risk loci for Alzheimer’s disease (AD). We recently reported that the bridging integrator 1 (BIN1) risk gene is linked to Tau pathology. Results We used glutathione S-transferase pull-down assays and nuclear magnetic resonance (NMR) experiments to demonstrate that BIN1 and Tau proteins interact directly and then map the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain (PRD) . Our NMR data showed that Tau phosphorylation at Thr231 weakens the SH3-PRD interaction. Using primary neurons, we found that BIN1-Tau complexes partly co-localize with the actin cytoskeleton; however, these complexes were not observed with Thr231-phosphorylated Tau species. Conclusion Our results show that (i) BIN1 and Tau bind through an SH3-PRD interaction and (ii) the interaction is downregulated by phosphorylation of Tau Thr231 (and potentially other residues). Our study sheds new light on regulation of the BIN1/Tau interaction and opens up new avenues for exploring its complex’s role in the pathogenesis of AD. © Sottejeau et al. 2015
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title_short	Tau phosphorylation regulates the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain
url	https://dx.doi.org/10.1186/s40478-015-0237-8
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author2	Bretteville, Alexis Cantrelle, François-Xavier Malmanche, Nicolas Demiaute, Florie Mendes, Tiago Delay, Charlotte Alves Dos Alves, Harmony Flaig, Amandine Davies, Peter Dourlen, Pierre Dermaut, Bart Laporte, Jocelyn Amouyel, Philippe Lippens, Guy Chapuis, Julien Landrieu, Isabelle Lambert, Jean-Charles
author2Str	Bretteville, Alexis Cantrelle, François-Xavier Malmanche, Nicolas Demiaute, Florie Mendes, Tiago Delay, Charlotte Alves Dos Alves, Harmony Flaig, Amandine Davies, Peter Dourlen, Pierre Dermaut, Bart Laporte, Jocelyn Amouyel, Philippe Lippens, Guy Chapuis, Julien Landrieu, Isabelle Lambert, Jean-Charles
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up_date	2024-07-03T18:03:38.014Z
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We recently reported that the bridging integrator 1 (BIN1) risk gene is linked to Tau pathology. Results We used glutathione S-transferase pull-down assays and nuclear magnetic resonance (NMR) experiments to demonstrate that BIN1 and Tau proteins interact directly and then map the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain (PRD) . Our NMR data showed that Tau phosphorylation at Thr231 weakens the SH3-PRD interaction. Using primary neurons, we found that BIN1-Tau complexes partly co-localize with the actin cytoskeleton; however, these complexes were not observed with Thr231-phosphorylated Tau species. Conclusion Our results show that (i) BIN1 and Tau bind through an SH3-PRD interaction and (ii) the interaction is downregulated by phosphorylation of Tau Thr231 (and potentially other residues). 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Tau phosphorylation regulates the interaction between BIN1’s SH3 domain and Tau’s proline-rich domain

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