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  • 1
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    Nuclear receptor Rev-erbalpha is a critical lithium-sensitive component of the circadian clock (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-18
    Description: Lithium is commonly used to treat bipolar disorder, which is associated with altered circadian rhythm. Lithium is a potent inhibitor of glycogen synthase kinase 3 (GSK3), which regulates circadian rhythm in several organisms. In experiments with cultured cells, we show here that GSK3beta phosphorylates and stabilizes the orphan nuclear receptor Rev-erbalpha, a negative component of the circadian clock. Lithium treatment of cells leads to rapid proteasomal degradation of Rev-erbalpha and activation of clock gene Bmal1. A form of Rev-erbalpha that is insensitive to lithium interferes with the expression of circadian genes. Control of Rev-erbalpha protein stability is thus a critical component of the peripheral clock and a biological target of lithium therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yin, Lei -- Wang, Jing -- Klein, Peter S -- Lazar, Mitchell A -- DK 19525/DK/NIDDK NIH HHS/ -- DK45586/DK/NIDDK NIH HHS/ -- MH058324/MH/NIMH NIH HHS/ -- R01 MH058324/MH/NIMH NIH HHS/ -- R01 MH058324-07/MH/NIMH NIH HHS/ -- R01 MH058324-08/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 17;311(5763):1002-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes, and Metabolism, and University of Pennsylvania School of Medicine, 415 Curie Boulevard, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484495" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Amino Acid Sequence ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; Biological Clocks/*physiology ; Cell Line ; Cell Line, Tumor ; Circadian Rhythm/*physiology ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Down-Regulation ; Gene Expression Regulation ; Glycogen Synthase Kinase 3/antagonists & inhibitors/metabolism ; Humans ; Lithium Chloride/*pharmacology ; Mice ; Molecular Sequence Data ; NIH 3T3 Cells ; Nuclear Receptor Subfamily 1, Group D, Member 1 ; Phosphorylation ; Promoter Regions, Genetic ; Proteasome Endopeptidase Complex/metabolism ; Proteasome Inhibitors ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*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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    Rev-erbalpha, a heme sensor that coordinates metabolic and circadian pathways (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-17
    Description: The circadian clock temporally coordinates metabolic homeostasis in mammals. Central to this is heme, an iron-containing porphyrin that serves as prosthetic group for enzymes involved in oxidative metabolism as well as transcription factors that regulate circadian rhythmicity. The circadian factor that integrates this dual function of heme is not known. We show that heme binds reversibly to the orphan nuclear receptor Rev-erbalpha, a critical negative component of the circadian core clock, and regulates its interaction with a nuclear receptor corepressor complex. Furthermore, heme suppresses hepatic gluconeogenic gene expression and glucose output through Rev-erbalpha-mediated gene repression. Thus, Rev-erbalpha serves as a heme sensor that coordinates the cellular clock, glucose homeostasis, and energy metabolism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yin, Lei -- Wu, Nan -- Curtin, Joshua C -- Qatanani, Mohammed -- Szwergold, Nava R -- Reid, Robert A -- Waitt, Gregory M -- Parks, Derek J -- Pearce, Kenneth H -- Wisely, G Bruce -- Lazar, Mitchell A -- R01 DK45586/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2007 Dec 14;318(5857):1786-9. Epub 2007 Nov 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18006707" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks ; Cell Line ; Cell Line, Tumor ; *Circadian Rhythm/genetics ; DNA-Binding Proteins/*metabolism ; Energy Metabolism ; *Gene Expression Regulation ; Gluconeogenesis/genetics ; Glucose/*metabolism ; Glucose-6-Phosphatase/genetics/metabolism ; Heme/*metabolism ; Hemin/pharmacology ; Histone Deacetylases/metabolism ; Homeostasis ; Humans ; Male ; *Metabolic Networks and Pathways ; Mice ; Nuclear Proteins/metabolism ; Nuclear Receptor Co-Repressor 1 ; Nuclear Receptor Subfamily 1, Group D, Member 1 ; Receptors, Cytoplasmic and Nuclear/*metabolism ; Repressor Proteins/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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  • 3
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    An immunosurveillance mechanism controls cancer cell ploidy (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-29
    Description: Cancer cells accommodate multiple genetic and epigenetic alterations that initially activate intrinsic (cell-autonomous) and extrinsic (immune-mediated) oncosuppressive mechanisms. Only once these barriers to oncogenesis have been overcome can malignant growth proceed unrestrained. Tetraploidization can contribute to oncogenesis because hyperploid cells are genomically unstable. We report that hyperploid cancer cells become immunogenic because of a constitutive endoplasmic reticulum stress response resulting in the aberrant cell surface exposure of calreticulin. Hyperploid, calreticulin-exposing cancer cells readily proliferated in immunodeficient mice and conserved their increased DNA content. In contrast, hyperploid cells injected into immunocompetent mice generated tumors only after a delay, and such tumors exhibited reduced DNA content, endoplasmic reticulum stress, and calreticulin exposure. Our results unveil an immunosurveillance system that imposes immunoselection against hyperploidy in carcinogen- and oncogene-induced cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Senovilla, Laura -- Vitale, Ilio -- Martins, Isabelle -- Tailler, Maximilien -- Pailleret, Claire -- Michaud, Mickael -- Galluzzi, Lorenzo -- Adjemian, Sandy -- Kepp, Oliver -- Niso-Santano, Mireia -- Shen, Shensi -- Marino, Guillermo -- Criollo, Alfredo -- Boileve, Alice -- Job, Bastien -- Ladoire, Sylvain -- Ghiringhelli, Francois -- Sistigu, Antonella -- Yamazaki, Takahiro -- Rello-Varona, Santiago -- Locher, Clara -- Poirier-Colame, Vichnou -- Talbot, Monique -- Valent, Alexander -- Berardinelli, Francesco -- Antoccia, Antonio -- Ciccosanti, Fabiola -- Fimia, Gian Maria -- Piacentini, Mauro -- Fueyo, Antonio -- Messina, Nicole L -- Li, Ming -- Chan, Christopher J -- Sigl, Verena -- Pourcher, Guillaume -- Ruckenstuhl, Christoph -- Carmona-Gutierrez, Didac -- Lazar, Vladimir -- Penninger, Josef M -- Madeo, Frank -- Lopez-Otin, Carlos -- Smyth, Mark J -- Zitvogel, Laurence -- Castedo, Maria -- Kroemer, Guido -- New York, N.Y. -- Science. 2012 Sep 28;337(6102):1678-84.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM, U848, Villejuif, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23019653" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calreticulin/immunology ; Cell Line, Tumor ; Common Variable Immunodeficiency/genetics ; DNA, Neoplasm/analysis/genetics ; Endoplasmic Reticulum Stress/*immunology ; Eukaryotic Initiation Factor-2/metabolism ; Humans ; Immunocompetence ; *Immunologic Surveillance ; Mice ; Mice, Inbred BALB C ; Neoplasms/chemically induced/*genetics/*immunology ; Phosphorylation ; *Ploidies
    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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