Abstract
A functional mouse CLOCK protein has long been thought to be essential for mammalian circadian clockwork function, based mainly on studies of mice bearing a dominant negative, antimorphic mutation in the Clock gene. However, new discoveries using recently developed Clock-null mutant mice have shaken up this view. In this review, I discuss how this recent work impacts and alters the previous view of the role of CLOCK in the mouse circadian clockwork.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Animals
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Basic Helix-Loop-Helix Transcription Factors / genetics
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Basic Helix-Loop-Helix Transcription Factors / physiology
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Biological Clocks / genetics*
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CLOCK Proteins
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Circadian Rhythm / genetics*
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Gene Expression Regulation / physiology
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Humans
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Mice / genetics*
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Mice / physiology
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Mice, Knockout
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Models, Biological
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Nerve Tissue Proteins / genetics
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Nerve Tissue Proteins / physiology
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Trans-Activators / genetics*
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Trans-Activators / physiology
Substances
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Basic Helix-Loop-Helix Transcription Factors
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Nerve Tissue Proteins
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Npas2 protein, mouse
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Trans-Activators
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CLOCK Proteins
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CLOCK protein, human
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Clock protein, mouse