The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Chantal Medina - One of the best experts on this subject based on the ideXlab platform.
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author correction defective gpsm2 gα i3 signalling disrupts stereocilia development and growth cone actin dynamics in chudley McCullough syndrome
Nature Communications, 2018Co-Authors: Stephanie A Mauriac, Yeri Esther Hien, Jonathan E Bird, Steve Dossantos Carvalho, Ronan Peyroutou, Sze Chim Lee, Maite M Moreau, Jeanmichel Blanc, Aysegul Gezer, Chantal MedinaAbstract:Nature Communications 8: Article number: 14907 (2017); Published: 7 April 2017; Updated: 25 May 2018 The original version of this Article contained an error in the spelling of the author Aysegul Gezer, which was incorrectly given as Aysegul Geyser. This has now been corrected in both the PDF and HTML versions of the Article.
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defective gpsm2 gαi3 signalling disrupts stereocilia development and growth cone actin dynamics in chudley McCullough syndrome
Nature Communications, 2017Co-Authors: Stephanie A Mauriac, Yeri Esther Hien, Jonathan E Bird, Steve Dossantos Carvalho, Ronan Peyroutou, Sze Chim Lee, Maite M Moreau, Jeanmichel Blanc, Aysegul Geyser, Chantal MedinaAbstract:Mutations in GPSM2 cause Chudley-McCullough syndrome (CMCS), an autosomal recessive neurological disorder characterized by early-onset sensorineural deafness and brain anomalies. Here, we show that mutation of the mouse orthologue of GPSM2 affects actin-rich stereocilia elongation in auditory and vestibular hair cells, causing deafness and balance defects. The G-protein subunit Gαi3, a well-documented partner of Gpsm2, participates in the elongation process, and its absence also causes hearing deficits. We show that Gpsm2 defines an ∼200 nm nanodomain at the tips of stereocilia and this localization requires the presence of Gαi3, myosin 15 and whirlin. Using single-molecule tracking, we report that loss of Gpsm2 leads to decreased outgrowth and a disruption of actin dynamics in neuronal growth cones. Our results elucidate the aetiology of CMCS and highlight a new molecular role for Gpsm2/Gαi3 in the regulation of actin dynamics in epithelial and neuronal tissues.
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defective gpsm2 gα i3 signalling disrupts stereocilia development and growth cone actin dynamics in chudley McCullough syndrome
Nature Communications, 2017Co-Authors: Stephanie A Mauriac, Yeri Esther Hien, Jonathan E Bird, Steve Dossantos Carvalho, Ronan Peyroutou, Sze Chim Lee, Maite M Moreau, Jeanmichel Blanc, Aysegul Geyser, Chantal MedinaAbstract:Mutations in GPSM2 cause Chudley-McCullough syndrome (CMCS), an autosomal recessive neurological disorder characterized by early-onset sensorineural deafness and brain anomalies. Here, we show that mutation of the mouse orthologue of GPSM2 affects actin-rich stereocilia elongation in auditory and vestibular hair cells, causing deafness and balance defects. The G-protein subunit Gαi3, a well-documented partner of Gpsm2, participates in the elongation process, and its absence also causes hearing deficits. We show that Gpsm2 defines an ∼200 nm nanodomain at the tips of stereocilia and this localization requires the presence of Gαi3, myosin 15 and whirlin. Using single-molecule tracking, we report that loss of Gpsm2 leads to decreased outgrowth and a disruption of actin dynamics in neuronal growth cones. Our results elucidate the aetiology of CMCS and highlight a new molecular role for Gpsm2/Gαi3 in the regulation of actin dynamics in epithelial and neuronal tissues.
Stephanie A Mauriac - One of the best experts on this subject based on the ideXlab platform.
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author correction defective gpsm2 gα i3 signalling disrupts stereocilia development and growth cone actin dynamics in chudley McCullough syndrome
Nature Communications, 2018Co-Authors: Stephanie A Mauriac, Yeri Esther Hien, Jonathan E Bird, Steve Dossantos Carvalho, Ronan Peyroutou, Sze Chim Lee, Maite M Moreau, Jeanmichel Blanc, Aysegul Gezer, Chantal MedinaAbstract:Nature Communications 8: Article number: 14907 (2017); Published: 7 April 2017; Updated: 25 May 2018 The original version of this Article contained an error in the spelling of the author Aysegul Gezer, which was incorrectly given as Aysegul Geyser. This has now been corrected in both the PDF and HTML versions of the Article.
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defective gpsm2 gαi3 signalling disrupts stereocilia development and growth cone actin dynamics in chudley McCullough syndrome
Nature Communications, 2017Co-Authors: Stephanie A Mauriac, Yeri Esther Hien, Jonathan E Bird, Steve Dossantos Carvalho, Ronan Peyroutou, Sze Chim Lee, Maite M Moreau, Jeanmichel Blanc, Aysegul Geyser, Chantal MedinaAbstract:Mutations in GPSM2 cause Chudley-McCullough syndrome (CMCS), an autosomal recessive neurological disorder characterized by early-onset sensorineural deafness and brain anomalies. Here, we show that mutation of the mouse orthologue of GPSM2 affects actin-rich stereocilia elongation in auditory and vestibular hair cells, causing deafness and balance defects. The G-protein subunit Gαi3, a well-documented partner of Gpsm2, participates in the elongation process, and its absence also causes hearing deficits. We show that Gpsm2 defines an ∼200 nm nanodomain at the tips of stereocilia and this localization requires the presence of Gαi3, myosin 15 and whirlin. Using single-molecule tracking, we report that loss of Gpsm2 leads to decreased outgrowth and a disruption of actin dynamics in neuronal growth cones. Our results elucidate the aetiology of CMCS and highlight a new molecular role for Gpsm2/Gαi3 in the regulation of actin dynamics in epithelial and neuronal tissues.
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defective gpsm2 gα i3 signalling disrupts stereocilia development and growth cone actin dynamics in chudley McCullough syndrome
Nature Communications, 2017Co-Authors: Stephanie A Mauriac, Yeri Esther Hien, Jonathan E Bird, Steve Dossantos Carvalho, Ronan Peyroutou, Sze Chim Lee, Maite M Moreau, Jeanmichel Blanc, Aysegul Geyser, Chantal MedinaAbstract:Mutations in GPSM2 cause Chudley-McCullough syndrome (CMCS), an autosomal recessive neurological disorder characterized by early-onset sensorineural deafness and brain anomalies. Here, we show that mutation of the mouse orthologue of GPSM2 affects actin-rich stereocilia elongation in auditory and vestibular hair cells, causing deafness and balance defects. The G-protein subunit Gαi3, a well-documented partner of Gpsm2, participates in the elongation process, and its absence also causes hearing deficits. We show that Gpsm2 defines an ∼200 nm nanodomain at the tips of stereocilia and this localization requires the presence of Gαi3, myosin 15 and whirlin. Using single-molecule tracking, we report that loss of Gpsm2 leads to decreased outgrowth and a disruption of actin dynamics in neuronal growth cones. Our results elucidate the aetiology of CMCS and highlight a new molecular role for Gpsm2/Gαi3 in the regulation of actin dynamics in epithelial and neuronal tissues.
Sze Chim Lee - One of the best experts on this subject based on the ideXlab platform.
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author correction defective gpsm2 gα i3 signalling disrupts stereocilia development and growth cone actin dynamics in chudley McCullough syndrome
Nature Communications, 2018Co-Authors: Stephanie A Mauriac, Yeri Esther Hien, Jonathan E Bird, Steve Dossantos Carvalho, Ronan Peyroutou, Sze Chim Lee, Maite M Moreau, Jeanmichel Blanc, Aysegul Gezer, Chantal MedinaAbstract:Nature Communications 8: Article number: 14907 (2017); Published: 7 April 2017; Updated: 25 May 2018 The original version of this Article contained an error in the spelling of the author Aysegul Gezer, which was incorrectly given as Aysegul Geyser. This has now been corrected in both the PDF and HTML versions of the Article.
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defective gpsm2 gαi3 signalling disrupts stereocilia development and growth cone actin dynamics in chudley McCullough syndrome
Nature Communications, 2017Co-Authors: Stephanie A Mauriac, Yeri Esther Hien, Jonathan E Bird, Steve Dossantos Carvalho, Ronan Peyroutou, Sze Chim Lee, Maite M Moreau, Jeanmichel Blanc, Aysegul Geyser, Chantal MedinaAbstract:Mutations in GPSM2 cause Chudley-McCullough syndrome (CMCS), an autosomal recessive neurological disorder characterized by early-onset sensorineural deafness and brain anomalies. Here, we show that mutation of the mouse orthologue of GPSM2 affects actin-rich stereocilia elongation in auditory and vestibular hair cells, causing deafness and balance defects. The G-protein subunit Gαi3, a well-documented partner of Gpsm2, participates in the elongation process, and its absence also causes hearing deficits. We show that Gpsm2 defines an ∼200 nm nanodomain at the tips of stereocilia and this localization requires the presence of Gαi3, myosin 15 and whirlin. Using single-molecule tracking, we report that loss of Gpsm2 leads to decreased outgrowth and a disruption of actin dynamics in neuronal growth cones. Our results elucidate the aetiology of CMCS and highlight a new molecular role for Gpsm2/Gαi3 in the regulation of actin dynamics in epithelial and neuronal tissues.
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defective gpsm2 gα i3 signalling disrupts stereocilia development and growth cone actin dynamics in chudley McCullough syndrome
Nature Communications, 2017Co-Authors: Stephanie A Mauriac, Yeri Esther Hien, Jonathan E Bird, Steve Dossantos Carvalho, Ronan Peyroutou, Sze Chim Lee, Maite M Moreau, Jeanmichel Blanc, Aysegul Geyser, Chantal MedinaAbstract:Mutations in GPSM2 cause Chudley-McCullough syndrome (CMCS), an autosomal recessive neurological disorder characterized by early-onset sensorineural deafness and brain anomalies. Here, we show that mutation of the mouse orthologue of GPSM2 affects actin-rich stereocilia elongation in auditory and vestibular hair cells, causing deafness and balance defects. The G-protein subunit Gαi3, a well-documented partner of Gpsm2, participates in the elongation process, and its absence also causes hearing deficits. We show that Gpsm2 defines an ∼200 nm nanodomain at the tips of stereocilia and this localization requires the presence of Gαi3, myosin 15 and whirlin. Using single-molecule tracking, we report that loss of Gpsm2 leads to decreased outgrowth and a disruption of actin dynamics in neuronal growth cones. Our results elucidate the aetiology of CMCS and highlight a new molecular role for Gpsm2/Gαi3 in the regulation of actin dynamics in epithelial and neuronal tissues.
Yeri Esther Hien - One of the best experts on this subject based on the ideXlab platform.
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author correction defective gpsm2 gα i3 signalling disrupts stereocilia development and growth cone actin dynamics in chudley McCullough syndrome
Nature Communications, 2018Co-Authors: Stephanie A Mauriac, Yeri Esther Hien, Jonathan E Bird, Steve Dossantos Carvalho, Ronan Peyroutou, Sze Chim Lee, Maite M Moreau, Jeanmichel Blanc, Aysegul Gezer, Chantal MedinaAbstract:Nature Communications 8: Article number: 14907 (2017); Published: 7 April 2017; Updated: 25 May 2018 The original version of this Article contained an error in the spelling of the author Aysegul Gezer, which was incorrectly given as Aysegul Geyser. This has now been corrected in both the PDF and HTML versions of the Article.
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defective gpsm2 gαi3 signalling disrupts stereocilia development and growth cone actin dynamics in chudley McCullough syndrome
Nature Communications, 2017Co-Authors: Stephanie A Mauriac, Yeri Esther Hien, Jonathan E Bird, Steve Dossantos Carvalho, Ronan Peyroutou, Sze Chim Lee, Maite M Moreau, Jeanmichel Blanc, Aysegul Geyser, Chantal MedinaAbstract:Mutations in GPSM2 cause Chudley-McCullough syndrome (CMCS), an autosomal recessive neurological disorder characterized by early-onset sensorineural deafness and brain anomalies. Here, we show that mutation of the mouse orthologue of GPSM2 affects actin-rich stereocilia elongation in auditory and vestibular hair cells, causing deafness and balance defects. The G-protein subunit Gαi3, a well-documented partner of Gpsm2, participates in the elongation process, and its absence also causes hearing deficits. We show that Gpsm2 defines an ∼200 nm nanodomain at the tips of stereocilia and this localization requires the presence of Gαi3, myosin 15 and whirlin. Using single-molecule tracking, we report that loss of Gpsm2 leads to decreased outgrowth and a disruption of actin dynamics in neuronal growth cones. Our results elucidate the aetiology of CMCS and highlight a new molecular role for Gpsm2/Gαi3 in the regulation of actin dynamics in epithelial and neuronal tissues.
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defective gpsm2 gα i3 signalling disrupts stereocilia development and growth cone actin dynamics in chudley McCullough syndrome
Nature Communications, 2017Co-Authors: Stephanie A Mauriac, Yeri Esther Hien, Jonathan E Bird, Steve Dossantos Carvalho, Ronan Peyroutou, Sze Chim Lee, Maite M Moreau, Jeanmichel Blanc, Aysegul Geyser, Chantal MedinaAbstract:Mutations in GPSM2 cause Chudley-McCullough syndrome (CMCS), an autosomal recessive neurological disorder characterized by early-onset sensorineural deafness and brain anomalies. Here, we show that mutation of the mouse orthologue of GPSM2 affects actin-rich stereocilia elongation in auditory and vestibular hair cells, causing deafness and balance defects. The G-protein subunit Gαi3, a well-documented partner of Gpsm2, participates in the elongation process, and its absence also causes hearing deficits. We show that Gpsm2 defines an ∼200 nm nanodomain at the tips of stereocilia and this localization requires the presence of Gαi3, myosin 15 and whirlin. Using single-molecule tracking, we report that loss of Gpsm2 leads to decreased outgrowth and a disruption of actin dynamics in neuronal growth cones. Our results elucidate the aetiology of CMCS and highlight a new molecular role for Gpsm2/Gαi3 in the regulation of actin dynamics in epithelial and neuronal tissues.
Jonathan E Bird - One of the best experts on this subject based on the ideXlab platform.
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author correction defective gpsm2 gα i3 signalling disrupts stereocilia development and growth cone actin dynamics in chudley McCullough syndrome
Nature Communications, 2018Co-Authors: Stephanie A Mauriac, Yeri Esther Hien, Jonathan E Bird, Steve Dossantos Carvalho, Ronan Peyroutou, Sze Chim Lee, Maite M Moreau, Jeanmichel Blanc, Aysegul Gezer, Chantal MedinaAbstract:Nature Communications 8: Article number: 14907 (2017); Published: 7 April 2017; Updated: 25 May 2018 The original version of this Article contained an error in the spelling of the author Aysegul Gezer, which was incorrectly given as Aysegul Geyser. This has now been corrected in both the PDF and HTML versions of the Article.
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defective gpsm2 gαi3 signalling disrupts stereocilia development and growth cone actin dynamics in chudley McCullough syndrome
Nature Communications, 2017Co-Authors: Stephanie A Mauriac, Yeri Esther Hien, Jonathan E Bird, Steve Dossantos Carvalho, Ronan Peyroutou, Sze Chim Lee, Maite M Moreau, Jeanmichel Blanc, Aysegul Geyser, Chantal MedinaAbstract:Mutations in GPSM2 cause Chudley-McCullough syndrome (CMCS), an autosomal recessive neurological disorder characterized by early-onset sensorineural deafness and brain anomalies. Here, we show that mutation of the mouse orthologue of GPSM2 affects actin-rich stereocilia elongation in auditory and vestibular hair cells, causing deafness and balance defects. The G-protein subunit Gαi3, a well-documented partner of Gpsm2, participates in the elongation process, and its absence also causes hearing deficits. We show that Gpsm2 defines an ∼200 nm nanodomain at the tips of stereocilia and this localization requires the presence of Gαi3, myosin 15 and whirlin. Using single-molecule tracking, we report that loss of Gpsm2 leads to decreased outgrowth and a disruption of actin dynamics in neuronal growth cones. Our results elucidate the aetiology of CMCS and highlight a new molecular role for Gpsm2/Gαi3 in the regulation of actin dynamics in epithelial and neuronal tissues.
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defective gpsm2 gα i3 signalling disrupts stereocilia development and growth cone actin dynamics in chudley McCullough syndrome
Nature Communications, 2017Co-Authors: Stephanie A Mauriac, Yeri Esther Hien, Jonathan E Bird, Steve Dossantos Carvalho, Ronan Peyroutou, Sze Chim Lee, Maite M Moreau, Jeanmichel Blanc, Aysegul Geyser, Chantal MedinaAbstract:Mutations in GPSM2 cause Chudley-McCullough syndrome (CMCS), an autosomal recessive neurological disorder characterized by early-onset sensorineural deafness and brain anomalies. Here, we show that mutation of the mouse orthologue of GPSM2 affects actin-rich stereocilia elongation in auditory and vestibular hair cells, causing deafness and balance defects. The G-protein subunit Gαi3, a well-documented partner of Gpsm2, participates in the elongation process, and its absence also causes hearing deficits. We show that Gpsm2 defines an ∼200 nm nanodomain at the tips of stereocilia and this localization requires the presence of Gαi3, myosin 15 and whirlin. Using single-molecule tracking, we report that loss of Gpsm2 leads to decreased outgrowth and a disruption of actin dynamics in neuronal growth cones. Our results elucidate the aetiology of CMCS and highlight a new molecular role for Gpsm2/Gαi3 in the regulation of actin dynamics in epithelial and neuronal tissues.