Protein CoAlation and antioxidant function of coenzyme A in prokaryotic cells

[1]  H. Sondermann,et al.  Timing and Reset Mechanism of GTP Hydrolysis-Driven Conformational Changes of Atlastin. , 2017, Structure.

[2]  Tina H Lee,et al.  The crossover conformational shift of the GTPase atlastin provides the energy driving ER fusion , 2017, The Journal of cell biology.

[3]  Tom A. Rapoport,et al.  Reconstitution of the tubular endoplasmic reticulum network with purified components , 2017, Nature.

[4]  T. Rapoport,et al.  Fusion of the endoplasmic reticulum by membrane-bound GTPases. , 2016, Seminars in cell & developmental biology.

[5]  Ben M. Webb,et al.  Comparative Protein Structure Modeling Using MODELLER , 2016, Current protocols in bioinformatics.

[6]  W. Prinz,et al.  Form follows function: the importance of endoplasmic reticulum shape. , 2015, Annual review of biochemistry.

[7]  Tina H Lee,et al.  ER network formation and membrane fusion by atlastin1/SPG3A disease variants , 2015, Molecular biology of the cell.

[8]  T. Rapoport,et al.  Cis and trans interactions between atlastin molecules during membrane fusion , 2015, Proceedings of the National Academy of Sciences.

[9]  Junjie Hu,et al.  Human atlastin GTPases mediate differentiated fusion of endoplasmic reticulum membranes , 2015, Protein & Cell.

[10]  B. Asselbergh,et al.  Developing 3D SEM in a broad biological context , 2015, Journal of microscopy.

[11]  Peijun Zhang,et al.  Membrane tethering by the atlastin GTPase depends on GTP hydrolysis but not on forming the cross-over configuration , 2014, Molecular biology of the cell.

[12]  I. Kurth,et al.  Membrane-shaping disorders: a common pathway in axon degeneration. , 2014, Brain : a journal of neurology.

[13]  T. Wieland,et al.  A novel missense mutation confirms ATL3 as a gene for hereditary sensory neuropathy type 1. , 2014, Brain : a journal of neurology.

[14]  S. Mundlos,et al.  Sensory neuropathy with bone destruction due to a mutation in the membrane-shaping atlastin GTPase 3. , 2014, Brain : a journal of neurology.

[15]  G. Voeltz,et al.  Endoplasmic reticulum structure and interconnections with other organelles. , 2013, Cold Spring Harbor perspectives in biology.

[16]  J. Veldink,et al.  ATL1 and REEP1 mutations in hereditary and sporadic upper motor neuron syndromes , 2013, Journal of Neurology.

[17]  W. Zipfel,et al.  Structural basis for conformational switching and GTP loading of the large G protein atlastin , 2013, The EMBO journal.

[18]  T. Rapoport,et al.  Lipid interaction of the C terminus and association of the transmembrane segments facilitate atlastin-mediated homotypic endoplasmic reticulum fusion , 2012, Proceedings of the National Academy of Sciences.

[19]  Johannes E. Schindelin,et al.  Fiji: an open-source platform for biological-image analysis , 2012, Nature Methods.

[20]  Kevin W Eliceiri,et al.  NIH Image to ImageJ: 25 years of image analysis , 2012, Nature Methods.

[21]  Peijun Zhang,et al.  An intramolecular salt bridge drives the soluble domain of GTP-bound atlastin into the postfusion conformation , 2011, The Journal of cell biology.

[22]  G. Knott,et al.  Focussed Ion Beam Milling and Scanning Electron Microscopy of Brain Tissue , 2011, Journal of visualized experiments : JoVE.

[23]  J. McNew,et al.  Membrane fusion by the GTPase atlastin requires a conserved C-terminal cytoplasmic tail and dimerization through the middle domain , 2011, Proceedings of the National Academy of Sciences.

[24]  M. Pericak-Vance,et al.  Mutation screening of spastin, atlastin, and REEP1 in hereditary spastic paraplegia , 2011, Clinical genetics.

[25]  Anne E Carpenter,et al.  Improved structure, function and compatibility for CellProfiler: modular high-throughput image analysis software , 2011, Bioinform..

[26]  T. Rapoport,et al.  Structures of the atlastin GTPase provide insight into homotypic fusion of endoplasmic reticulum membranes , 2011, Proceedings of the National Academy of Sciences.

[27]  H. Sondermann,et al.  Structural basis for the nucleotide-dependent dimerization of the large G protein atlastin-1/SPG3A , 2011, Proceedings of the National Academy of Sciences.

[28]  C. Blackstone,et al.  Targeted high-throughput sequencing identifies mutations in atlastin-1 as a cause of hereditary sensory neuropathy type I. , 2011, American journal of human genetics.

[29]  Arrate Muñoz-Barrutia,et al.  3D reconstruction of histological sections: Application to mammary gland tissue , 2010, Microscopy research and technique.

[30]  Yoko Shibata,et al.  A Class of Dynamin-like GTPases Involved in the Generation of the Tubular ER Network , 2009, Cell.

[31]  A. Martinuzzi,et al.  Homotypic fusion of ER membranes requires the dynamin-like GTPase Atlastin , 2009, Nature.

[32]  A. Verkhratsky,et al.  A lentivirally delivered photoactivatable GFP to assess continuity in the endoplasmic reticulum of neurones and glia , 2009, Pflügers Archiv - European Journal of Physiology.

[33]  C. Blackstone,et al.  Atlastin GTPases are required for Golgi apparatus and ER morphogenesis. , 2008, Human molecular genetics.

[34]  Rodrigo Lopez,et al.  Clustal W and Clustal X version 2.0 , 2007, Bioinform..

[35]  M. Ruberg,et al.  Mutations in the SPG3A gene encoding the GTPase atlastin interfere with vesicle trafficking in the ER/Golgi interface and Golgi morphogenesis , 2007, Molecular and Cellular Neuroscience.

[36]  D. Trono,et al.  Production and Titration of Lentiviral Vectors , 2006, Current protocols in neuroscience.

[37]  Conrad C. Huang,et al.  UCSF Chimera—A visualization system for exploratory research and analysis , 2004, J. Comput. Chem..

[38]  P. Hedera,et al.  Mutations in a newly identified GTPase gene cause autosomal dominant hereditary spastic paraplegia , 2001, Nature Genetics.

[39]  N. Greenfield.  Using circular dichroism spectra to estimate protein secondary structure , 2007, Nature Protocols.