Abstract
Heterodimers of CLOCK and BMAL1, bHLH-PAS transcription factors, are believed to be the major transcriptional regulators of the circadian clock mechanism in mammals. However, a recent study shows that CLOCK-deficient mice continue to exhibit robust behavioral and molecular rhythms. Here we report that the transcription factor NPAS2 (MOP4) is able to functionally substitute for CLOCK in the master brain clock in mice to regulate circadian rhythmicity.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Analysis of Variance
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Animals
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Basic Helix-Loop-Helix Transcription Factors / deficiency
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Basic Helix-Loop-Helix Transcription Factors / metabolism*
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Behavior, Animal
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CLOCK Proteins
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Circadian Rhythm / physiology*
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Gene Expression Regulation / genetics
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Mice
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Mice, Knockout
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Motor Activity / genetics
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Nerve Tissue Proteins / deficiency
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Nerve Tissue Proteins / metabolism*
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Suprachiasmatic Nucleus / physiology*
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Trans-Activators / deficiency
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Trans-Activators / metabolism*
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, mouse