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  • 1
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    AMPK regulates the circadian clock by cryptochrome phosphorylation and degradation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-17
    Description: Circadian clocks coordinate behavioral and physiological processes with daily light-dark cycles by driving rhythmic transcription of thousands of genes. Whereas the master clock in the brain is set by light, pacemakers in peripheral organs, such as the liver, are reset by food availability, although the setting, or "entrainment," mechanisms remain mysterious. Studying mouse fibroblasts, we demonstrated that the nutrient-responsive adenosine monophosphate-activated protein kinase (AMPK) phosphorylates and destabilizes the clock component cryptochrome 1 (CRY1). In mouse livers, AMPK activity and nuclear localization were rhythmic and inversely correlated with CRY1 nuclear protein abundance. Stimulation of AMPK destabilized cryptochromes and altered circadian rhythms, and mice in which the AMPK pathway was genetically disrupted showed alterations in peripheral clocks. Thus, phosphorylation by AMPK enables cryptochrome to transduce nutrient signals to circadian clocks in mammalian peripheral organs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2819106/" 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/PMC2819106/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamia, Katja A -- Sachdeva, Uma M -- DiTacchio, Luciano -- Williams, Elliot C -- Alvarez, Jacqueline G -- Egan, Daniel F -- Vasquez, Debbie S -- Juguilon, Henry -- Panda, Satchidananda -- Shaw, Reuben J -- Thompson, Craig B -- Evans, Ronald M -- CA104838/CA/NCI NIH HHS/ -- DK057978/DK/NIDDK NIH HHS/ -- DK062434/DK/NIDDK NIH HHS/ -- DK080425/DK/NIDDK NIH HHS/ -- EY016807/EY/NEI NIH HHS/ -- P01 CA104838/CA/NCI NIH HHS/ -- P01 CA104838-05S1/CA/NCI NIH HHS/ -- P30 CA014195/CA/NCI NIH HHS/ -- R01 DK080425/DK/NIDDK NIH HHS/ -- R01 DK080425-03/DK/NIDDK NIH HHS/ -- R01 EY016807/EY/NEI NIH HHS/ -- R01 EY016807-03/EY/NEI NIH HHS/ -- R37 DK057978/DK/NIDDK NIH HHS/ -- R37 DK057978-31/DK/NIDDK NIH HHS/ -- T32 HL007439/HL/NHLBI NIH HHS/ -- T32 HL007439-27/HL/NHLBI NIH HHS/ -- T32-HL07439-27/HL/NHLBI NIH HHS/ -- U19 DK062434/DK/NIDDK NIH HHS/ -- U19 DK062434-08S19002/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Oct 16;326(5951):437-40. doi: 10.1126/science.1172156.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Expression Laboratory, the Salk Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19833968" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/*metabolism ; ARNTL Transcription Factors ; Amino Acid Substitution ; Aminoimidazole Carboxamide/analogs & derivatives/pharmacology ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Cell Line ; Cell Nucleus/metabolism ; Cells, Cultured ; Circadian Rhythm/*physiology ; Cryptochromes ; Culture Media ; Flavoproteins/genetics/*metabolism ; Food ; Glucose/metabolism/pharmacology ; Humans ; Liver/*metabolism ; Mice ; Mutagenesis, Site-Directed ; Mutant Proteins/metabolism ; Phosphorylation ; Promoter Regions, Genetic ; Protein Stability ; Recombinant Fusion Proteins/metabolism ; Ribonucleotides/pharmacology ; Signal Transduction
    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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    Phosphorylation of ULK1 (hATG1) by AMP-activated protein kinase connects energy sensing to mitophagy (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-06
    Description: Adenosine monophosphate-activated protein kinase (AMPK) is a conserved sensor of intracellular energy activated in response to low nutrient availability and environmental stress. In a screen for conserved substrates of AMPK, we identified ULK1 and ULK2, mammalian orthologs of the yeast protein kinase Atg1, which is required for autophagy. Genetic analysis of AMPK or ULK1 in mammalian liver and Caenorhabditis elegans revealed a requirement for these kinases in autophagy. In mammals, loss of AMPK or ULK1 resulted in aberrant accumulation of the autophagy adaptor p62 and defective mitophagy. Reconstitution of ULK1-deficient cells with a mutant ULK1 that cannot be phosphorylated by AMPK revealed that such phosphorylation is required for mitochondrial homeostasis and cell survival during starvation. These findings uncover a conserved biochemical mechanism coupling nutrient status with autophagy and cell survival.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3030664/" 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/PMC3030664/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Egan, Daniel F -- Shackelford, David B -- Mihaylova, Maria M -- Gelino, Sara -- Kohnz, Rebecca A -- Mair, William -- Vasquez, Debbie S -- Joshi, Aashish -- Gwinn, Dana M -- Taylor, Rebecca -- Asara, John M -- Fitzpatrick, James -- Dillin, Andrew -- Viollet, Benoit -- Kundu, Mondira -- Hansen, Malene -- Shaw, Reuben J -- 1P01CA120964/CA/NCI NIH HHS/ -- 1P01CA120964-01A/CA/NCI NIH HHS/ -- 5P30CA006516-43/CA/NCI NIH HHS/ -- P01 CA120964/CA/NCI NIH HHS/ -- P01 CA120964-05/CA/NCI NIH HHS/ -- P30 CA006516/CA/NCI NIH HHS/ -- P30 CA006516-43/CA/NCI NIH HHS/ -- P30CA014195/CA/NCI NIH HHS/ -- R01 DK080425/DK/NIDDK NIH HHS/ -- R01 DK080425-04/DK/NIDDK NIH HHS/ -- R01 DK080425-05/DK/NIDDK NIH HHS/ -- T32 CA009370/CA/NCI NIH HHS/ -- T32 CA009370-29/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Jan 28;331(6016):456-61. doi: 10.1126/science.1196371. Epub 2010 Dec 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Cell Biology Laboratory, Dulbecco Center for Cancer Research, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21205641" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/*metabolism ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; *Autophagy ; Caenorhabditis elegans/metabolism ; Caenorhabditis elegans Proteins/genetics/metabolism ; Cell Line ; Cell Line, Tumor ; Cell Survival ; Energy Metabolism ; Hepatocytes/metabolism ; Humans ; Insulin/metabolism ; Intracellular Signaling Peptides and Proteins/chemistry/genetics/*metabolism ; Liver/metabolism ; Metformin/pharmacology ; Mice ; Mitochondria, Liver/metabolism/ultrastructure ; Phenformin/pharmacology ; Phosphorylation ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Signal Transduction ; Transcription Factors/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)
    Location Call Number Expected Availability
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