The GTPase domain of gamma-tubulin is required for normal mitochondrial function and spatial organization
Lisa Lindström et al. find that the gamma-tubulin cellular network is required to maintain mitochondrial function and organization in the cell. Knockdown of gamma-tubulin or loss of its GTPase domain disrupts the mitochondrial network and alters respiratory capacity and expression of mitochondrial g...
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2018-05-01
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Series: | Communications Biology |
Online Access: | https://doi.org/10.1038/s42003-018-0037-3 |
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doaj-d8b682b135e44aecbc719b783aa778cd2020-12-07T23:51:22ZengNature Publishing GroupCommunications Biology2399-36422018-05-011111810.1038/s42003-018-0037-3The GTPase domain of gamma-tubulin is required for normal mitochondrial function and spatial organizationLisa Lindström0Tongbin Li1Darina Malycheva2Arun Kancharla3Helén Nilsson4Neelanjan Vishnu5Hindrik Mulder6Martin Johansson7Catalina Ana Rosselló8Maria Alvarado-Kristensson9Molecular Pathology, Department of Translational Medicine, Lund University, Skåne University Hospital MalmöAccuraScience LLCMolecular Pathology, Department of Translational Medicine, Lund University, Skåne University Hospital MalmöMolecular Pathology, Department of Translational Medicine, Lund University, Skåne University Hospital MalmöPathology, Department of Translational Medicine, Lund University, Skåne University Hospital MalmöUnit of Molecular Metabolism, Lund University Diabetes Centre MalmöUnit of Molecular Metabolism, Lund University Diabetes Centre MalmöPathology, Department of Translational Medicine, Lund University, Skåne University Hospital MalmöMolecular Pathology, Department of Translational Medicine, Lund University, Skåne University Hospital MalmöMolecular Pathology, Department of Translational Medicine, Lund University, Skåne University Hospital MalmöLisa Lindström et al. find that the gamma-tubulin cellular network is required to maintain mitochondrial function and organization in the cell. Knockdown of gamma-tubulin or loss of its GTPase domain disrupts the mitochondrial network and alters respiratory capacity and expression of mitochondrial genes.https://doi.org/10.1038/s42003-018-0037-3 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Lisa Lindström Tongbin Li Darina Malycheva Arun Kancharla Helén Nilsson Neelanjan Vishnu Hindrik Mulder Martin Johansson Catalina Ana Rosselló Maria Alvarado-Kristensson |
spellingShingle |
Lisa Lindström Tongbin Li Darina Malycheva Arun Kancharla Helén Nilsson Neelanjan Vishnu Hindrik Mulder Martin Johansson Catalina Ana Rosselló Maria Alvarado-Kristensson The GTPase domain of gamma-tubulin is required for normal mitochondrial function and spatial organization Communications Biology |
author_facet |
Lisa Lindström Tongbin Li Darina Malycheva Arun Kancharla Helén Nilsson Neelanjan Vishnu Hindrik Mulder Martin Johansson Catalina Ana Rosselló Maria Alvarado-Kristensson |
author_sort |
Lisa Lindström |
title |
The GTPase domain of gamma-tubulin is required for normal mitochondrial function and spatial organization |
title_short |
The GTPase domain of gamma-tubulin is required for normal mitochondrial function and spatial organization |
title_full |
The GTPase domain of gamma-tubulin is required for normal mitochondrial function and spatial organization |
title_fullStr |
The GTPase domain of gamma-tubulin is required for normal mitochondrial function and spatial organization |
title_full_unstemmed |
The GTPase domain of gamma-tubulin is required for normal mitochondrial function and spatial organization |
title_sort |
gtpase domain of gamma-tubulin is required for normal mitochondrial function and spatial organization |
publisher |
Nature Publishing Group |
series |
Communications Biology |
issn |
2399-3642 |
publishDate |
2018-05-01 |
description |
Lisa Lindström et al. find that the gamma-tubulin cellular network is required to maintain mitochondrial function and organization in the cell. Knockdown of gamma-tubulin or loss of its GTPase domain disrupts the mitochondrial network and alters respiratory capacity and expression of mitochondrial genes. |
url |
https://doi.org/10.1038/s42003-018-0037-3 |
work_keys_str_mv |
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