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  • 1
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    Requirement of mammalian Timeless for circadian rhythmicity (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-18
    Description: Despite a central circadian role in Drosophila for the transcriptional regulator Timeless (dTim), the relevance of mammalian Timeless (mTim) remains equivocal. Conditional knockdown of mTim protein expression in the rat suprachiasmatic nucleus (SCN) disrupted SCN neuronal activity rhythms, and altered levels of known core clock elements. Full-length mTim protein (mTIM-fl) exhibited a 24-hour oscillation, where as a truncated isoform (mTIM-s) was constitutively expressed. mTIM-fl associated with the mammalian clock Period proteins (mPERs) in oscillating SCN cells. These data suggest that mTim is required for rhythmicity and is a functional homolog of dTim on the negative-feedback arm of the mammalian molecular clockwork.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnes, Jessica W -- Tischkau, Shelley A -- Barnes, Jeffrey A -- Mitchell, Jennifer W -- Burgoon, Penny W -- Hickok, Jason R -- Gillette, Martha U -- GM07143/GM/NIGMS NIH HHS/ -- HL67007/HL/NHLBI NIH HHS/ -- NS10170/NS/NINDS NIH HHS/ -- NS11134/NS/NINDS NIH HHS/ -- NS11158/NS/NINDS NIH HHS/ -- NS22155/NS/NINDS NIH HHS/ -- NS35859/NS/NINDS NIH HHS/ -- R01 HL067007/HL/NHLBI NIH HHS/ -- R01 NS022155/NS/NINDS NIH HHS/ -- R01 NS035859/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 17;302(5644):439-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Structural Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14564007" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks ; Cell Cycle Proteins ; Cell Line ; *Circadian Rhythm ; Cryptochromes ; *Drosophila Proteins ; Electrophysiology ; *Eye Proteins ; Flavoproteins/metabolism ; Humans ; In Vitro Techniques ; Intracellular Signaling Peptides and Proteins ; Neurons/physiology ; Nuclear Proteins/metabolism ; Oligonucleotides, Antisense/pharmacology ; Period Circadian Proteins ; *Photoreceptor Cells, Invertebrate ; RNA Interference ; RNA, Messenger/genetics/metabolism ; Rats ; Rats, Inbred Strains ; Receptors, G-Protein-Coupled ; Reverse Transcriptase Polymerase Chain Reaction ; Suprachiasmatic Nucleus/*physiology ; Transcription Factors/chemistry/genetics/*metabolism ; Transfection
    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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    Biodiversity meets the atmosphere: a global view of forest canopies (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-12
    Description: The forest canopy is the functional interface between 90% of Earth's terrestrial biomass and the atmosphere. Multidisciplinary research in the canopy has expanded concepts of global species richness, physiological processes, and the provision of ecosystem services. Trees respond in a species-specific manner to elevated carbon dioxide levels, while climate change threatens plant-animal interactions in the canopy and will likely alter the production of biogenic aerosols that affect cloud formation and atmospheric chemistry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ozanne, C M P -- Anhuf, D -- Boulter, S L -- Keller, M -- Kitching, R L -- Korner, C -- Meinzer, F C -- Mitchell, A W -- Nakashizuka, T -- Dias, P L Silva -- Stork, N E -- Wright, S J -- Yoshimura, M -- New York, N.Y. -- Science. 2003 Jul 11;301(5630):183-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Research in Ecology and Environment, School of Life and Sport Sciences, University of Surrey Roehampton, West Hill, London SW15 3SN, UK. c.ozanne@roehampton.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12855799" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Atmosphere ; Biomass ; Climate ; *Ecosystem ; Environment ; *Plant Leaves/physiology ; Sunlight ; *Trees/growth & development
    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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    Cell biology. Reversible centriole depletion with an inhibitor of Polo-like kinase 4 (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-05-02
    Description: Centrioles are ancient organelles that build centrosomes, the major microtubule-organizing centers of animal cells. Extra centrosomes are a common feature of cancer cells. To investigate the importance of centrosomes in the proliferation of normal and cancer cells, we developed centrinone, a reversible inhibitor of Polo-like kinase 4 (Plk4), a serine-threonine protein kinase that initiates centriole assembly. Centrinone treatment caused centrosome depletion in human and other vertebrate cells. Centrosome loss irreversibly arrested normal cells in a senescence-like G1 state by a p53-dependent mechanism that was independent of DNA damage, stress, Hippo signaling, extended mitotic duration, or segregation errors. In contrast, cancer cell lines with normal or amplified centrosome numbers could proliferate indefinitely after centrosome loss. Upon centrinone washout, each cancer cell line returned to an intrinsic centrosome number "set point." Thus, cells with cancer-associated mutations fundamentally differ from normal cells in their response to centrosome loss.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4764081/" 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/PMC4764081/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wong, Yao Liang -- Anzola, John V -- Davis, Robert L -- Yoon, Michelle -- Motamedi, Amir -- Kroll, Ashley -- Seo, Chanmee P -- Hsia, Judy E -- Kim, Sun K -- Mitchell, Jennifer W -- Mitchell, Brian J -- Desai, Arshad -- Gahman, Timothy C -- Shiau, Andrew K -- Oegema, Karen -- GM074207/GM/NIGMS NIH HHS/ -- GM089970/GM/NIGMS NIH HHS/ -- GM103403/GM/NIGMS NIH HHS/ -- R01 GM089970/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2015 Jun 5;348(6239):1155-60. doi: 10.1126/science.aaa5111. Epub 2015 Apr 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Medicine, Ludwig Institute for Cancer Research, University of California, San Diego, La Jolla, CA 92093, USA. ; Small Molecule Discovery Program, Ludwig Institute for Cancer Research, La Jolla, CA 92093, USA. ; Department of Cell and Molecular Biology, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA. ; Small Molecule Discovery Program, Ludwig Institute for Cancer Research, La Jolla, CA 92093, USA. koegema@ucsd.edu ashiau@ucsd.edu. ; Department of Cellular and Molecular Medicine, Ludwig Institute for Cancer Research, University of California, San Diego, La Jolla, CA 92093, USA. koegema@ucsd.edu ashiau@ucsd.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25931445" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; Cell Proliferation ; Centrioles/*drug effects ; Humans ; Mice ; Piperazines/pharmacology ; Protein Kinase Inhibitors/chemistry/*pharmacology ; Protein-Serine-Threonine Kinases/*antagonists & inhibitors ; Pyrimidines/chemistry/*pharmacology ; Sulfones/chemistry/*pharmacology
    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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