Modulation of Rab GTPase function by a protein phosphocholine transferase
Shaeri Mukherjee,
Xiaoyun Liu,
Kohei Arasaki,
Justin McDonough,
Jorge E. Galán and
Craig R. Roy ()
Additional contact information
Shaeri Mukherjee: Section of Microbial Pathogenesis, Yale University School of Medicine, Boyer Center for Molecular Medicine, Yale University, 295 Congress Avenue, New Haven, Connecticut, CT-06536, USA
Xiaoyun Liu: Section of Microbial Pathogenesis, Yale University School of Medicine, Boyer Center for Molecular Medicine, Yale University, 295 Congress Avenue, New Haven, Connecticut, CT-06536, USA
Kohei Arasaki: Section of Microbial Pathogenesis, Yale University School of Medicine, Boyer Center for Molecular Medicine, Yale University, 295 Congress Avenue, New Haven, Connecticut, CT-06536, USA
Justin McDonough: Section of Microbial Pathogenesis, Yale University School of Medicine, Boyer Center for Molecular Medicine, Yale University, 295 Congress Avenue, New Haven, Connecticut, CT-06536, USA
Jorge E. Galán: Section of Microbial Pathogenesis, Yale University School of Medicine, Boyer Center for Molecular Medicine, Yale University, 295 Congress Avenue, New Haven, Connecticut, CT-06536, USA
Craig R. Roy: Section of Microbial Pathogenesis, Yale University School of Medicine, Boyer Center for Molecular Medicine, Yale University, 295 Congress Avenue, New Haven, Connecticut, CT-06536, USA
Nature, 2011, vol. 477, issue 7362, 103-106
Abstract:
Novel role for phosphocholination The pathogen that causes legionnaires' disease, Legionella pneumophila, secretes proteins into host cells that target Rab GTPases involved in vesicular trafficking, thereby enhancing intracellular replication. It is now shown that the L. pneumophila effector protein AnkX modifies Rab1 through a novel protein modification — phosphocholination.
Date: 2011
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DOI: 10.1038/nature10335
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