Abstract
In mammals, transcriptional autorepression by Period (PER) and Cryptochrome (CRY) protein complexes is essential for the generation of circadian rhythms. We have identified CAVIN-3 as a new, cytoplasmic PER2-interacting protein influencing circadian clock properties. Thus, CAVIN-3 loss- and gain-of-function shortened and lengthened, respectively, the circadian period in fibroblasts and affected PER:CRY protein abundance and interaction. While depletion of protein kinase Cδ (PKCδ), a known partner of CAVIN-3, had little effect on circadian gene expression, CAVIN-3 required the PKCδ-binding site to exert its effect on period length. This suggests the involvement of yet uncharacterized protein kinases. Finally, CAVIN-3 activity in circadian gene expression was independent of caveolae.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Caveolae / metabolism
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Circadian Clocks / genetics*
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Circadian Clocks / physiology
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Cryptochromes* / genetics
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Cryptochromes* / metabolism
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Gene Expression Regulation
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Intracellular Signaling Peptides and Proteins / genetics*
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Intracellular Signaling Peptides and Proteins / metabolism*
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Membrane Proteins* / genetics
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Membrane Proteins* / metabolism
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Mice
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NIH 3T3 Cells
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Period Circadian Proteins* / genetics
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Period Circadian Proteins* / metabolism
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Protein Binding
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Protein Kinase C-delta / metabolism
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Protein Transport / genetics
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RNA-Binding Proteins
Substances
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CAVIN3 protein, human
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Cavin1 protein, mouse
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Cry2 protein, mouse
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Cryptochromes
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Intracellular Signaling Peptides and Proteins
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Membrane Proteins
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Per2 protein, mouse
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Period Circadian Proteins
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RNA-Binding Proteins
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Protein Kinase C-delta