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  • 1
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    Sequence interpretation. Functional annotation of mouse genome sequences (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-03-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nadeau, J H -- Balling, R -- Barsh, G -- Beier, D -- Brown, S D -- Bucan, M -- Camper, S -- Carlson, G -- Copeland, N -- Eppig, J -- Fletcher, C -- Frankel, W N -- Ganten, D -- Goldowitz, D -- Goodnow, C -- Guenet, J L -- Hicks, G -- Hrabe de Angelis, M -- Jackson, I -- Jacob, H J -- Jenkins, N -- Johnson, D -- Justice, M -- Kay, S -- Kingsley, D -- Lehrach, H -- Magnuson, T -- Meisler, M -- Poustka, A -- Rinchik, E M -- Rossant, J -- Russell, L B -- Schimenti, J -- Shiroishi, T -- Skarnes, W C -- Soriano, P -- Stanford, W -- Takahashi, J S -- Wurst, W -- Zimmer, A -- International Mouse Mutagenesis Consortium -- New York, N.Y. -- Science. 2001 Feb 16;291(5507):1251-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, BRB 624, Case Western Reserve University School of Medicine, 10900 Euclid Avenue, Cleveland, OH 44106, USA. jhn4@po.cwru.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11233449" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; *Computational Biology ; Costs and Cost Analysis ; Genes/physiology ; Genetic Techniques ; *Genome ; *Genomics ; International Cooperation ; Mice/*genetics ; Mutagenesis ; Mutation ; Phenotype ; Private Sector ; Public Sector ; Research Support as Topic ; *Sequence Analysis, DNA
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Role of the CLOCK protein in the mammalian circadian mechanism (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-11
    Description: The mouse Clock gene encodes a bHLH-PAS protein that regulates circadian rhythms and is related to transcription factors that act as heterodimers. Potential partners of CLOCK were isolated in a two-hybrid screen, and one, BMAL1, was coexpressed with CLOCK and PER1 at known circadian clock sites in brain and retina. CLOCK-BMAL1 heterodimers activated transcription from E-box elements, a type of transcription factor-binding site, found adjacent to the mouse per1 gene and from an identical E-box known to be important for per gene expression in Drosophila. Mutant CLOCK from the dominant-negative Clock allele and BMAL1 formed heterodimers that bound DNA but failed to activate transcription. Thus, CLOCK-BMAL1 heterodimers appear to drive the positive component of per transcriptional oscillations, which are thought to underlie circadian rhythmicity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gekakis, N -- Staknis, D -- Nguyen, H B -- Davis, F C -- Wilsbacher, L D -- King, D P -- Takahashi, J S -- Weitz, C J -- New York, N.Y. -- Science. 1998 Jun 5;280(5369):1564-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston MA 02115, USA. 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9616112" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; Biological Clocks ; CLOCK Proteins ; Cell Cycle Proteins ; Circadian Rhythm/genetics/*physiology ; Cloning, Molecular ; Cricetinae ; DNA/metabolism ; Dimerization ; Feedback ; Gene Expression ; Helix-Loop-Helix Motifs ; Male ; Mesocricetus ; Mice ; Mutation ; Nuclear Proteins/*genetics/metabolism ; Period Circadian Proteins ; Promoter Regions, Genetic ; Retina/metabolism ; Suprachiasmatic Nucleus/metabolism ; Trans-Activators/genetics/*metabolism ; Transcription Factors/genetics/*metabolism ; *Transcriptional Activation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Narcolepsy genes wake up the sleep field (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takahashi, J S -- New York, N.Y. -- Science. 1999 Sep 24;285(5436):2076-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208-3520, USA. j-takahashi@nwu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523205" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; Circadian Rhythm ; Cloning, Molecular ; Dogs ; Homeostasis ; Hypothalamus/metabolism ; Ligands ; Mice ; Mice, Knockout ; Narcolepsy/*genetics/physiopathology ; Neurons/metabolism ; Neuropeptides/metabolism ; Orexin Receptors ; Receptors, G-Protein-Coupled ; Receptors, Neuropeptide/chemistry/*genetics/physiology ; *Sleep/physiology ; Sleep, REM
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Positional syntenic cloning and functional characterization of the mammalian circadian mutation tau (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-25
    Description: The tau mutation is a semidominant autosomal allele that dramatically shortens period length of circadian rhythms in Syrian hamsters. We report the molecular identification of the tau locus using genetically directed representational difference analysis to define a region of conserved synteny in hamsters with both the mouse and human genomes. The tau locus is encoded by casein kinase I epsilon (CKIepsilon), a homolog of the Drosophila circadian gene double-time. In vitro expression and functional studies of wild-type and tau mutant CKIepsilon enzyme reveal that the mutant enzyme has a markedly reduced maximal velocity and autophosphorylation state. In addition, in vitro CKIepsilon can interact with mammalian PERIOD proteins, and the mutant enzyme is deficient in its ability to phosphorylate PERIOD. We conclude that tau is an allele of hamster CKIepsilon and propose a mechanism by which the mutation leads to the observed aberrant circadian phenotype in mutant animals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3869379/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3869379/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lowrey, P L -- Shimomura, K -- Antoch, M P -- Yamazaki, S -- Zemenides, P D -- Ralph, M R -- Menaker, M -- Takahashi, J S -- R01MH56647/MH/NIMH NIH HHS/ -- R37MH39592/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2000 Apr 21;288(5465):483-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Physiology, Howard Hughes Medical Institute, Northwestern University, Evanston, IL 60208, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10775102" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Casein Kinases ; Cell Cycle Proteins ; Chromosome Mapping ; *Circadian Rhythm/genetics ; Cloning, Molecular ; Cricetinae ; Female ; Heterozygote ; Humans ; Male ; Mesocricetus ; Mice ; Microsatellite Repeats ; Molecular Sequence Data ; Nuclear Proteins/genetics/metabolism ; Period Circadian Proteins ; Phenotype ; Phosphorylation ; *Point Mutation ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Protein Kinases/chemistry/*genetics/*metabolism ; RNA, Messenger/genetics/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Suprachiasmatic Nucleus/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Role of mouse cryptochrome blue-light photoreceptor in circadian photoresponses (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-20
    Description: Cryptochromes are photoactive pigments in the eye that have been proposed to function as circadian photopigments. Mice lacking the cryptochrome 2 blue-light photoreceptor gene (mCry2) were tested for circadian clock-related functions. The mutant mice had a lower sensitivity to acute light induction of mPer1 in the suprachiasmatic nucleus (SCN) but exhibited normal circadian oscillations of mPer1 and mCry1 messenger RNA in the SCN. Behaviorally, the mutants had an intrinsic circadian period about 1 hour longer than normal and exhibited high-amplitude phase shifts in response to light pulses administered at circadian time 17. These data are consistent with the hypothesis that CRY2 protein modulates circadian responses in mice and suggest that cryptochromes have a role in circadian photoreception in mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thresher, R J -- Vitaterna, M H -- Miyamoto, Y -- Kazantsev, A -- Hsu, D S -- Petit, C -- Selby, C P -- Dawut, L -- Smithies, O -- Takahashi, J S -- Sancar, A -- GM20069/GM/NIGMS NIH HHS/ -- GM31082/GM/NIGMS NIH HHS/ -- P0 AG11412/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1998 Nov 20;282(5393):1490-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9822380" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle Proteins ; Circadian Rhythm/*physiology ; Cryptochromes ; *Drosophila Proteins ; *Eye Proteins ; Female ; Flavoproteins/genetics/*physiology ; Gene Expression Regulation ; Gene Targeting ; In Situ Hybridization ; *Light ; Male ; Mice ; Mice, Inbred C57BL ; Motor Activity ; Mutation ; Nuclear Proteins/genetics ; Period Circadian Proteins ; *Photoreceptor Cells, Invertebrate ; Photoreceptor Cells, Vertebrate/*physiology ; Receptors, G-Protein-Coupled ; Suprachiasmatic Nucleus/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Disruption of the clock components CLOCK and BMAL1 leads to hypoinsulinaemia and diabetes (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-06-22
    Description: The molecular clock maintains energy constancy by producing circadian oscillations of rate-limiting enzymes involved in tissue metabolism across the day and night. During periods of feeding, pancreatic islets secrete insulin to maintain glucose homeostasis, and although rhythmic control of insulin release is recognized to be dysregulated in humans with diabetes, it is not known how the circadian clock may affect this process. Here we show that pancreatic islets possess self-sustained circadian gene and protein oscillations of the transcription factors CLOCK and BMAL1. The phase of oscillation of islet genes involved in growth, glucose metabolism and insulin signalling is delayed in circadian mutant mice, and both Clock and Bmal1 (also called Arntl) mutants show impaired glucose tolerance, reduced insulin secretion and defects in size and proliferation of pancreatic islets that worsen with age. Clock disruption leads to transcriptome-wide alterations in the expression of islet genes involved in growth, survival and synaptic vesicle assembly. Notably, conditional ablation of the pancreatic clock causes diabetes mellitus due to defective beta-cell function at the very latest stage of stimulus-secretion coupling. These results demonstrate a role for the beta-cell clock in coordinating insulin secretion with the sleep-wake cycle, and reveal that ablation of the pancreatic clock can trigger the onset of diabetes mellitus.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2920067/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2920067/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marcheva, Biliana -- Ramsey, Kathryn Moynihan -- Buhr, Ethan D -- Kobayashi, Yumiko -- Su, Hong -- Ko, Caroline H -- Ivanova, Ganka -- Omura, Chiaki -- Mo, Shelley -- Vitaterna, Martha H -- Lopez, James P -- Philipson, Louis H -- Bradfield, Christopher A -- Crosby, Seth D -- JeBailey, Lellean -- Wang, Xiaozhong -- Takahashi, Joseph S -- Bass, Joseph -- P01 AG011412/AG/NIA NIH HHS/ -- P01 AG011412-080011/AG/NIA NIH HHS/ -- R01 HL097817/HL/NHLBI NIH HHS/ -- R01 HL097817-01/HL/NHLBI NIH HHS/ -- R37 ES005703/ES/NIEHS NIH HHS/ -- R37-ES-005703/ES/NIEHS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Jul 29;466(7306):627-31. doi: 10.1038/nature09253.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20562852" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/deficiency/*genetics/metabolism ; Aging/genetics/pathology ; Animals ; Blood Glucose/analysis/metabolism ; CLOCK Proteins/deficiency/*genetics/metabolism ; Cell Proliferation ; Cell Size ; Cell Survival ; Circadian Rhythm/genetics/*physiology ; Diabetes Mellitus/genetics/*metabolism ; Gene Expression Profiling ; Glucose Intolerance/genetics ; Glucose Tolerance Test ; In Vitro Techniques ; Insulin/*blood/metabolism/secretion ; Islets of Langerhans/*metabolism/pathology/secretion ; Mice ; Period Circadian Proteins/genetics/metabolism ; Phenotype ; Sleep/genetics/physiology ; Synaptic Vesicles/metabolism ; Wakefulness/genetics/physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 7
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    Regulation of jun-B messenger RNA and AP-1 activity by light and a circadian clock (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-20
    Description: The suprachiasmatic nuclei (SCN) of the hypothalamus comprise the primary pacemaker responsible for generation of circadian rhythms in mammals. Light stimuli that synchronize this circadian clock induce expression of the c-fos gene in rodent SCN, which suggests a possible role for Fos in circadian entrainment. Appropriate light stimuli also induce the expression of jun-B messenger RNA in the SCN of golden hamsters but only slightly elevate c-jun messenger RNA levels. In addition, light increases the amount of a protein complex in the SCN that binds specifically to sites on DNA known to mediate regulation by the AP-1 transcription factor. The photic regulation of both jun-B messenger RNA expression and AP-1 binding activity is dependent on circadian phase: only light stimuli that shift behavioral rhythms induce jun-B and AP-1 expression. Thus, light and the circadian pacemaker interact to regulate a specific set of immediate-early genes in the SCN that may participate in entrainment of the circadian clock.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kornhauser, J M -- Nelson, D E -- Mayo, K E -- Takahashi, J S -- New York, N.Y. -- Science. 1992 Mar 20;255(5051):1581-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Neuroscience, Northwestern University, Evanston, IL 60208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1549784" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cricetinae ; *Gene Expression Regulation ; Genes, fos/physiology ; Genes, jun/*physiology ; *Light ; Molecular Sequence Data ; Nucleic Acid Hybridization ; *Periodicity ; Proto-Oncogene Proteins c-jun/*biosynthesis ; RNA Probes ; RNA, Messenger/*biosynthesis ; Suprachiasmatic Nucleus/physiology ; Time Factors ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    cAMP-dependent signaling as a core component of the mammalian circadian pacemaker (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-20
    Description: The mammalian circadian clockwork is modeled as transcriptional and posttranslational feedback loops, whereby circadian genes are periodically suppressed by their protein products. We show that adenosine 3',5'-monophosphate (cAMP) signaling constitutes an additional, bona fide component of the oscillatory network. cAMP signaling is rhythmic and sustains the transcriptional loop of the suprachiasmatic nucleus, determining canonical pacemaker properties of amplitude, phase, and period. This role is general and is evident in peripheral mammalian tissues and cell lines, which reveals an unanticipated point of circadian regulation in mammals qualitatively different from the existing transcriptional feedback model. We propose that daily activation of cAMP signaling, driven by the transcriptional oscillator, in turn sustains progression of transcriptional rhythms. In this way, clock output constitutes an input to subsequent cycles.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2735813/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2735813/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Neill, John S -- Maywood, Elizabeth S -- Chesham, Johanna E -- Takahashi, Joseph S -- Hastings, Michael H -- MC_U105170643/Medical Research Council/United Kingdom -- U.1051.02.004(78799)/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Howard Hughes Medical Institute/ -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2008 May 16;320(5878):949-53. doi: 10.1126/science.1152506.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18487196" target="_blank"〉PubMed〈/a〉
    Keywords: Adenine/analogs & derivatives/pharmacology ; Adenylyl Cyclase Inhibitors ; Adenylyl Cyclases/metabolism ; Animals ; Biological Clocks/genetics/*physiology ; Cell Cycle Proteins/genetics/metabolism ; Circadian Rhythm/drug effects/genetics/*physiology ; Cyclic AMP/*metabolism ; Enzyme Inhibitors/pharmacology ; Feedback, Physiological ; Gene Expression Regulation/drug effects ; Guanine Nucleotide Exchange Factors/metabolism ; Mice ; Mice, Transgenic ; NIH 3T3 Cells ; Nuclear Proteins/genetics/metabolism ; Period Circadian Proteins ; Response Elements ; *Signal Transduction ; Suprachiasmatic Nucleus/drug effects/*metabolism ; Transcription Factors/genetics/metabolism ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Temperature as a universal resetting cue for mammalian circadian oscillators (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-16
    Description: Environmental temperature cycles are a universal entraining cue for all circadian systems at the organismal level with the exception of homeothermic vertebrates. We report here that resistance to temperature entrainment is a property of the suprachiasmatic nucleus (SCN) network and is not a cell-autonomous property of mammalian clocks. This differential sensitivity to temperature allows the SCN to drive circadian rhythms in body temperature, which can then act as a universal cue for the entrainment of cell-autonomous oscillators throughout the body. Pharmacological experiments show that network interactions in the SCN are required for temperature resistance and that the heat shock pathway is integral to temperature resetting and temperature compensation in mammalian cells. These results suggest that the evolutionarily ancient temperature resetting response can be used in homeothermic animals to enhance internal circadian synchronization.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3625727/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3625727/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buhr, Ethan D -- Yoo, Seung-Hee -- Takahashi, Joseph S -- P50 MH074924/MH/NIMH NIH HHS/ -- P50 MH074924-01/MH/NIMH NIH HHS/ -- P50 MH074924-02/MH/NIMH NIH HHS/ -- P50 MH074924-03/MH/NIMH NIH HHS/ -- P50 MH074924-04/MH/NIMH NIH HHS/ -- P50 MH074924-05/MH/NIMH NIH HHS/ -- T32 AG 20418/AG/NIA NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Oct 15;330(6002):379-85. doi: 10.1126/science.1195262.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208-3520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20947768" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine Vasopressin/metabolism ; Benzhydryl Compounds/pharmacology ; Biological Clocks/*physiology ; *Body Temperature ; Body Temperature Regulation ; Calcium Channels, L-Type/physiology ; Cell Communication ; Circadian Rhythm/*physiology ; Cues ; DNA-Binding Proteins/metabolism ; Heat-Shock Response ; Lung/physiology ; Mice ; Pituitary Gland/physiology ; Pyrrolidinones/pharmacology ; Signal Transduction ; Suprachiasmatic Nucleus/cytology/*physiology ; Temperature ; Tissue Culture Techniques ; Transcription Factors/metabolism ; Transcription, Genetic/drug effects ; Vasoactive Intestinal Peptide/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Crystal structure of the heterodimeric CLOCK:BMAL1 transcriptional activator complex (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-02
    Description: The circadian clock in mammals is driven by an autoregulatory transcriptional feedback mechanism that takes approximately 24 hours to complete. A key component of this mechanism is a heterodimeric transcriptional activator consisting of two basic helix-loop-helix PER-ARNT-SIM (bHLH-PAS) domain protein subunits, CLOCK and BMAL1. Here, we report the crystal structure of a complex containing the mouse CLOCK:BMAL1 bHLH-PAS domains at 2.3 A resolution. The structure reveals an unusual asymmetric heterodimer with the three domains in each of the two subunits--bHLH, PAS-A, and PAS-B--tightly intertwined and involved in dimerization interactions, resulting in three distinct protein interfaces. Mutations that perturb the observed heterodimer interfaces affect the stability and activity of the CLOCK:BMAL1 complex as well as the periodicity of the circadian oscillator. The structure of the CLOCK:BMAL1 complex is a starting point for understanding at an atomic level the mechanism driving the mammalian circadian clock.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694778/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694778/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Nian -- Chelliah, Yogarany -- Shan, Yongli -- Taylor, Clinton A -- Yoo, Seung-Hee -- Partch, Carrie -- Green, Carla B -- Zhang, Hong -- Takahashi, Joseph S -- R01 GM081875/GM/NIGMS NIH HHS/ -- R01 GM090247/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Jul 13;337(6091):189-94. doi: 10.1126/science.1222804. Epub 2012 May 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22653727" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/*chemistry/genetics/metabolism ; Amino Acid Sequence ; Animals ; CLOCK Proteins/*chemistry/genetics/metabolism ; Cells, Cultured ; *Circadian Rhythm ; Crystallography, X-Ray ; DNA/metabolism ; HEK293 Cells ; Helix-Loop-Helix Motifs ; Humans ; Mice ; Models, Molecular ; Molecular Sequence Data ; Mutant Proteins/chemistry/metabolism ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Multimerization ; Protein Structure, Quaternary ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Protein Subunits/chemistry/metabolism ; Static Electricity ; *Transcriptional Activation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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