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  • 1
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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
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Transplanted suprachiasmatic nucleus determines circadian period (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-23
    Description: The pacemaker role of the suprachiasmatic nucleus in a mammalian circadian system was tested by neural transplantation by using a mutant strain of hamster that shows a short circadian period. Small neural grafts from the suprachiasmatic region restored circadian rhythms to arrhythmic animals whose own nucleus had been ablated. The restored rhythms always exhibited the period of the donor genotype regardless of the direction of the transplant or genotype of the host. The basic period of the overt circadian rhythm therefore is determined by cells of the suprachiasmatic region.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ralph, M R -- Foster, R G -- Davis, F C -- Menaker, M -- HD13162/HD/NICHD NIH HHS/ -- HD18686/HD/NICHD NIH HHS/ -- MH09483/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 23;247(4945):975-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Virginia, Charlottesville 22903.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2305266" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Circadian Rhythm/genetics/*physiology ; Cricetinae ; Immunohistochemistry ; Male ; Mutation ; Nerve Tissue/*transplantation ; Neuropeptide Y/analysis ; Suprachiasmatic Nucleus/embryology/*physiology ; Vasopressins/analysis
    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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  • 3
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    A mutation of the circadian system in golden hamsters (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-02
    Description: A mutation has been found that dramatically shortens the period of the circadian locomotor rhythm of golden hamsters. The pattern of inheritance of this mutation suggests that it occurred at a single, autosomal locus (tau). Wild-type animals have rhythms with free-running periods averaging about 24 hours; animals heterozygous for the mutation have periods of about 22 hours, whereas homozygous animals have rhythms with periods close to 20 hours. Animals that carry the mutant alleles exhibit abnormal entrainment to 24-hour light:dark cycles or are unable to entrain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ralph, M R -- Menaker, M -- HD 13162/HD/NICHD NIH HHS/ -- MH 09483/MH/NIMH NIH HHS/ -- MH 17148/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 2;241(4870):1225-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neuroscience, University of Oregon, Eugene 97403.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3413487" target="_blank"〉PubMed〈/a〉
    Keywords: *Activity Cycles ; Animals ; *Circadian Rhythm ; Cricetinae/*genetics ; Heterozygote ; Homozygote ; Light ; Male ; Mesocricetus/*genetics/physiology ; Motor Activity/physiology ; Mutation ; Periodicity ; Phenotype
    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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  • 4
    Electronic Resource
    Electronic Resource
    The circadian system of c-fos deficient mice (1996)
    Springer
    Journal of comparative physiology 178 (1996), S. 563-570 
    Details
    ISSN: 1432-1351
    Keywords: Circadian rhythm ; Gene targeting ; Phase shift ; Entrainment ; Light cycle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract We examined the role of c-fos in the synchronization of circadian rhythms to environmental light cycles using a line of gene-targeted mice carrying a null mutation at this locus. Circadian locomotor rhythms in mutants had similar periods as wild-type controls but took significantly longer than controls to entrain to 12:12 light-dark cycles. Light-induced phase shifts of rhythms in constant dark were attenuated in mutants although the circadian timing of phase delays and advances was not changed. A functional retinohypothalamic projection was indicated from behavioral results and light-induced jun-B expression in the SCN. The results indicate that while c-fos activation is not an absolute requirement for rhythm generation nor photic responses, it is required for normal entrainment of the mammalian biological clock.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00190186
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  • 5
    Electronic Resource
    Electronic Resource
    Phase response curve to anisomycin intau mutant hamsters (1992)
    Springer
    Cellular and molecular life sciences 48 (1992), S. 875-877 
    Details
    ISSN: 1420-9071
    Keywords: Activity ; anisomycin ; hamster ; non-photic ; phase response curve ; protein synthesis ; rhythms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Administration of the protein synthesis inhibitor, anisomycin, to wild type hamsters produces phase shifts in their circadian rhythms that have similarities to shifts produced by non-photic behavioral stimulation. A mutation that shortens the period of rhythms in hamsters results in altered responsiveness to non-photic input. However, responses of the mutants to anisomycin are unaffected: their phase response curve (PRC) for anisomycin is similar to that of wild types. This suggests that 1) anisomycin is not acting on mechanisms specifically involved in non-photic behavioral phase shifting, and 2) the mutation affects the non-photic input pathway or the pacemaker itself at a point that is upstream from anisomycin's site of action.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02118423
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  • 6
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    Mania-like behavior induced by genetic dysfunction of the neuron-specific Na+,K+-ATPase  3 sodium pump (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-10-24
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 7
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    Mania-like behavior induced by genetic dysfunction of the neuron-specific Na+,K+-ATPase {alpha}3 sodium pump [Neuroscience] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-11-02
    Description: Bipolar disorder is a debilitating psychopathology with unknown etiology. Accumulating evidence suggests the possible involvement of Na+,K+-ATPase dysfunction in the pathophysiology of bipolar disorder. Here we show that Myshkin mice carrying an inactivating mutation in the neuron-specific Na+,K+-ATPase α3 subunit display a behavioral profile remarkably similar to bipolar patients in the manic state. Myshkin mice show increased Ca2+ signaling in cultured cortical neurons and phospho-activation of extracellular signal regulated kinase (ERK) and Akt in the hippocampus. The mood-stabilizing drugs lithium and valproic acid, specific ERK inhibitor SL327, rostafuroxin, and transgenic expression of a functional Na+,K+-ATPase α3 protein rescue the mania-like phenotype of Myshkin mice. These findings establish Myshkin mice as a unique model of mania, reveal an important role for Na+,K+-ATPase α3 in the control of mania-like behavior, and identify Na+,K+-ATPase α3, its physiological regulators and downstream signal transduction pathways as putative targets for the design of new antimanic therapies.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 8
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    Phase response curve to anisomycin intau mutant hamsters (1992)
    Springer
    Details
    Publication Date: 1992-09-01
    Print ISSN: 0014-4754
    Topics: Biology , Medicine
    Published by Springer
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