Abstract
Defects in protein trafficking within the cell body and cilia are thought to underlie the human disease Bardet-Biedl syndrome (BBS). In this issue, Nachury et al. (2007) reveal that a large complex of proteins implicated in BBS cooperates with Rabin8-the GTP exchange factor for the small GTPase Rab8-to promote cilia formation and presumably movement of membrane proteins from the cell into the cilium.
Publication types
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Research Support, Non-U.S. Gov't
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Comment
MeSH terms
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Animals
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Bardet-Biedl Syndrome / metabolism*
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Biological Transport*
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Cilia / metabolism*
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Flagella
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GTP Phosphohydrolases / metabolism
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Humans
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Microtubules / metabolism
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Models, Biological
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Protein Binding
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Protein Transport
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rab GTP-Binding Proteins / metabolism
Substances
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GTP Phosphohydrolases
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RAB8A protein, human
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rab GTP-Binding Proteins