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  • 1
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    Immune homeostasis enforced by co-localized effector and regulatory T cells (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-11-26
    Description: FOXP3(+) regulatory T cells (Treg cells) prevent autoimmunity by limiting the effector activity of T cells that have escaped thymic negative selection or peripheral inactivation. Despite the information available about molecular factors mediating the suppressive function of Treg cells, the relevant cellular events in intact tissues remain largely unexplored, and whether Treg cells prevent activation of self-specific T cells or primarily limit damage from such cells has not been determined. Here we use multiplex, quantitative imaging in mice to show that, within secondary lymphoid tissues, highly suppressive Treg cells expressing phosphorylated STAT5 exist in discrete clusters with rare IL-2-positive T cells that are activated by self-antigens. This local IL-2 induction of STAT5 phosphorylation in Treg cells is part of a feedback circuit that limits further autoimmune responses. Inducible ablation of T cell receptor expression by Treg cells reduces their regulatory capacity and disrupts their localization in clusters, resulting in uncontrolled effector T cell responses. Our data thus reveal that autoreactive T cells are activated to cytokine production on a regular basis, with physically co-clustering T cell receptor-stimulated Treg cells responding in a negative feedback manner to suppress incipient autoimmunity and maintain immune homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4702500/" 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/PMC4702500/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Zhiduo -- Gerner, Michael Y -- Van Panhuys, Nicholas -- Levine, Andrew G -- Rudensky, Alexander Y -- Germain, Ronald N -- R37 AI034206/AI/NIAID NIH HHS/ -- R37AI034206/AI/NIAID NIH HHS/ -- T32GM007739/GM/NIGMS NIH HHS/ -- Z01 AI000403-25/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Dec 10;528(7581):225-30. doi: 10.1038/nature16169. Epub 2015 Nov 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphocyte Biology Section, Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-1892, USA. ; Howard Hughes Medical Institute, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA. ; Immunology Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26605524" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Movement ; Dendritic Cells/cytology/immunology ; Female ; Gene Expression Regulation ; Homeostasis/*immunology ; Mice ; Mice, Inbred C57BL ; Phenotype ; Protein Transport ; STAT5 Transcription Factor/metabolism ; T-Lymphocytes, Regulatory/*immunology
    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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  • 2
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    Tet2 is required to resolve inflammation by recruiting Hdac2 to specifically repress IL-6 (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-08-20
    Description: Epigenetic modifiers have fundamental roles in defining unique cellular identity through the establishment and maintenance of lineage-specific chromatin and methylation status. Several DNA modifications such as 5-hydroxymethylcytosine (5hmC) are catalysed by the ten eleven translocation (Tet) methylcytosine dioxygenase family members, and the roles of Tet proteins in regulating chromatin architecture and gene transcription independently of DNA methylation have been gradually uncovered. However, the regulation of immunity and inflammation by Tet proteins independent of their role in modulating DNA methylation remains largely unknown. Here we show that Tet2 selectively mediates active repression of interleukin-6 (IL-6) transcription during inflammation resolution in innate myeloid cells, including dendritic cells and macrophages. Loss of Tet2 resulted in the upregulation of several inflammatory mediators, including IL-6, at late phase during the response to lipopolysaccharide challenge. Tet2-deficient mice were more susceptible to endotoxin shock and dextran-sulfate-sodium-induced colitis, displaying a more severe inflammatory phenotype and increased IL-6 production compared to wild-type mice. IkappaBzeta, an IL-6-specific transcription factor, mediated specific targeting of Tet2 to the Il6 promoter, further indicating opposite regulatory roles of IkappaBzeta at initial and resolution phases of inflammation. For the repression mechanism, independent of DNA methylation and hydroxymethylation, Tet2 recruited Hdac2 and repressed transcription of Il6 via histone deacetylation. We provide mechanistic evidence for the gene-specific transcription repression activity of Tet2 via histone deacetylation and for the prevention of constant transcription activation at the chromatin level for resolving inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4697747/" 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/PMC4697747/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Qian -- Zhao, Kai -- Shen, Qicong -- Han, Yanmei -- Gu, Yan -- Li, Xia -- Zhao, Dezhi -- Liu, Yiqi -- Wang, Chunmei -- Zhang, Xiang -- Su, Xiaoping -- Liu, Juan -- Ge, Wei -- Levine, Ross L -- Li, Nan -- Cao, Xuetao -- P30 CA008748/CA/NCI NIH HHS/ -- R01 CA173636/CA/NCI NIH HHS/ -- England -- Nature. 2015 Sep 17;525(7569):389-93. doi: 10.1038/nature15252. Epub 2015 Aug 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Key Laboratory of Medical Molecular Biology &Department of Immunology, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100005, China. ; National Key Laboratory of Medical Immunology &Institute of Immunology, Second Military Medical University, Shanghai 200433, China. ; Human Oncology and Pathogenesis Program and Leukemia Service, Department of Medicine, Memorial Sloan-Kettering Cancer, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26287468" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Chromatin/chemistry/genetics/metabolism ; Colitis/enzymology/immunology/metabolism ; DNA Methylation ; DNA-Binding Proteins/deficiency/*metabolism ; Dendritic Cells/cytology/metabolism ; Down-Regulation/genetics ; Epigenesis, Genetic ; Female ; HEK293 Cells ; Histone Deacetylase 2/*metabolism ; Histones/chemistry/metabolism ; Humans ; I-kappa B Proteins/metabolism ; Inflammation/enzymology/immunology/*metabolism ; Interleukin-6/*antagonists & inhibitors/*biosynthesis/genetics/immunology ; Macrophages/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Promoter Regions, Genetic/genetics ; Proto-Oncogene Proteins/deficiency/*metabolism ; Transcription, Genetic
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Antibody-mediated clearance of alphavirus infection from neurons (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-08
    Description: Humoral immunity is important for protection against viral infection and neutralization of extracellular virus, but clearance of virus from infected tissues is thought to be mediated solely by cellular immunity. However, in a SCID mouse model of persistent alphavirus encephalomyelitis, adoptive transfer of hyperimmune serum resulted in clearance of infectious virus and viral RNA from the nervous system, whereas adoptive transfer of sensitized T lymphocytes had no effect on viral replication. Three monoclonal antibodies to two different epitopes on the E2 envelope glycoprotein mediated viral clearance. Treatment of alphavirus-infected primary cultured rat neurons with these monoclonal antibodies to E2 resulted in decreased viral protein synthesis, followed by gradual termination of mature infectious virion production. Thus, antibody can mediate clearance of alphavirus infection from neurons by restricting viral gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levine, B -- Hardwick, J M -- Trapp, B D -- Crawford, T O -- Bollinger, R C -- Griffin, D E -- NS29234/NS/NINDS NIH HHS/ -- T32-NS-07000/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Nov 8;254(5033):856-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1658936" target="_blank"〉PubMed〈/a〉
    Keywords: Alphavirus/immunology/isolation & purification/*physiology ; Animals ; Antibodies, Monoclonal/*therapeutic use ; Central Nervous System/immunology/*microbiology ; Encephalomyelitis/*immunology/microbiology/therapy ; *Immunotherapy, Adoptive ; Mice ; Mice, Inbred Strains ; Mice, SCID ; Neurons/immunology/*microbiology ; RNA, Viral/isolation & purification ; T-Lymphocytes/*immunology ; Togaviridae Infections/*immunology/therapy ; Virus Replication
    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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    Receptor activation alters inner surface potential during phagocytosis (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-07-22
    Description: The surface potential of biological membranes varies according to their lipid composition. We devised genetically encoded probes to assess surface potential in intact cells. These probes revealed marked, localized alterations in the charge of the inner surface of the plasma membrane of macrophages during the course of phagocytosis. Hydrolysis of phosphoinositides and displacement of phosphatidylserine accounted for the change in surface potential at the phagosomal cup. Signaling molecules such as K-Ras, Rac1, and c-Src that are targeted to the membrane by electrostatic interactions were rapidly released from membrane subdomains where the surface charge was altered by lipid remodeling during phagocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yeung, Tony -- Terebiznik, Mauricio -- Yu, Liming -- Silvius, John -- Abidi, Wasif M -- Philips, Mark -- Levine, Tim -- Kapus, Andras -- Grinstein, Sergio -- New York, N.Y. -- Science. 2006 Jul 21;313(5785):347-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Biology, Hepatology, and Nutrition Department, Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16857939" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Cell Line ; Cell Membrane/*physiology ; Fluorescent Dyes/metabolism ; Hydrophobic and Hydrophilic Interactions ; Immunoglobulin G/immunology ; Ionomycin/pharmacology ; Lipid Bilayers/metabolism ; Liposomes/metabolism ; Macrophages/*physiology ; Membrane Potentials ; Mice ; Molecular Probes/metabolism ; Neuropeptides/metabolism ; Opsonin Proteins ; Peptides/metabolism ; *Phagocytosis ; Phagosomes/physiology ; Phospholipids/analysis/metabolism ; Receptors, Fc/immunology/metabolism ; Static Electricity ; rac GTP-Binding Proteins/metabolism ; rac1 GTP-Binding Protein ; ras Proteins/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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    Acetylcholine-synthesizing T cells relay neural signals in a vagus nerve circuit (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-09-17
    Description: Neural circuits regulate cytokine production to prevent potentially damaging inflammation. A prototypical vagus nerve circuit, the inflammatory reflex, inhibits tumor necrosis factor-alpha production in spleen by a mechanism requiring acetylcholine signaling through the alpha7 nicotinic acetylcholine receptor expressed on cytokine-producing macrophages. Nerve fibers in spleen lack the enzymatic machinery necessary for acetylcholine production; therefore, how does this neural circuit terminate in cholinergic signaling? We identified an acetylcholine-producing, memory phenotype T cell population in mice that is integral to the inflammatory reflex. These acetylcholine-producing T cells are required for inhibition of cytokine production by vagus nerve stimulation. Thus, action potentials originating in the vagus nerve regulate T cells, which in turn produce the neurotransmitter, acetylcholine, required to control innate immune responses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4548937/" 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/PMC4548937/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosas-Ballina, Mauricio -- Olofsson, Peder S -- Ochani, Mahendar -- Valdes-Ferrer, Sergio I -- Levine, Yaakov A -- Reardon, Colin -- Tusche, Michael W -- Pavlov, Valentin A -- Andersson, Ulf -- Chavan, Sangeeta -- Mak, Tak W -- Tracey, Kevin J -- R01 GM057226/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Oct 7;334(6052):98-101. doi: 10.1126/science.1209985. Epub 2011 Sep 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, New York 11030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21921156" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/*biosynthesis ; Action Potentials ; Animals ; CD4-Positive T-Lymphocytes/*immunology/*metabolism ; Choline O-Acetyltransferase/metabolism ; Cholinergic Agents/metabolism ; Female ; *Immunity, Innate ; Immunologic Memory ; Inflammation ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; *Neuroimmunomodulation ; Norepinephrine/pharmacology ; Receptors, Nicotinic/metabolism ; Signal Transduction ; Spleen/immunology/innervation/metabolism ; T-Lymphocyte Subsets/immunology/metabolism ; Tumor Necrosis Factor-alpha/blood ; Vagus Nerve/*physiology ; Vagus Nerve Stimulation ; alpha7 Nicotinic Acetylcholine Receptor
    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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    Akt-mediated regulation of autophagy and tumorigenesis through Beclin 1 phosphorylation (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-01
    Description: Aberrant signaling through the class I phosphatidylinositol 3-kinase (PI3K)-Akt axis is frequent in human cancer. Here, we show that Beclin 1, an essential autophagy and tumor suppressor protein, is a target of the protein kinase Akt. Expression of a Beclin 1 mutant resistant to Akt-mediated phosphorylation increased autophagy, reduced anchorage-independent growth, and inhibited Akt-driven tumorigenesis. Akt-mediated phosphorylation of Beclin 1 enhanced its interactions with 14-3-3 and vimentin intermediate filament proteins, and vimentin depletion increased autophagy and inhibited Akt-driven transformation. Thus, Akt-mediated phosphorylation of Beclin 1 functions in autophagy inhibition, oncogenesis, and the formation of an autophagy-inhibitory Beclin 1/14-3-3/vimentin intermediate filament complex. These findings have broad implications for understanding the role of Akt signaling and intermediate filament proteins in autophagy and cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3507442/" 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/PMC3507442/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Richard C -- Wei, Yongjie -- An, Zhenyi -- Zou, Zhongju -- Xiao, Guanghua -- Bhagat, Govind -- White, Michael -- Reichelt, Julia -- Levine, Beth -- K08 CA164047/CA/NCI NIH HHS/ -- P30 CA142543/CA/NCI NIH HHS/ -- R01 CA071443/CA/NCI NIH HHS/ -- R01 CA084254/CA/NCI NIH HHS/ -- R01 CA109618/CA/NCI NIH HHS/ -- R01 CA129451/CA/NCI NIH HHS/ -- R01 CA84254-S1/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Nov 16;338(6109):956-9. doi: 10.1126/science.1225967. Epub 2012 Oct 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, 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/23112296" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis Regulatory Proteins/genetics/*metabolism ; *Autophagy ; Cell Line, Tumor ; Cell Transformation, Neoplastic/genetics/*metabolism ; Fibroblasts/metabolism/pathology ; HeLa Cells ; Humans ; Membrane Proteins/genetics/*metabolism ; Mice ; Phosphorylation ; Proto-Oncogene Proteins c-akt/genetics/*metabolism ; RNA, Small Interfering/genetics ; Rats ; Transduction, Genetic ; Vimentin/genetics ; Xenograft Model Antitumor Assays
    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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  • 7
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    Circadian clock NAD+ cycle drives mitochondrial oxidative metabolism in mice (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-09-21
    Description: Circadian clocks are self-sustained cellular oscillators that synchronize oxidative and reductive cycles in anticipation of the solar cycle. We found that the clock transcription feedback loop produces cycles of nicotinamide adenine dinucleotide (NAD(+)) biosynthesis, adenosine triphosphate production, and mitochondrial respiration through modulation of mitochondrial protein acetylation to synchronize oxidative metabolic pathways with the 24-hour fasting and feeding cycle. Circadian control of the activity of the NAD(+)-dependent deacetylase sirtuin 3 (SIRT3) generated rhythms in the acetylation and activity of oxidative enzymes and respiration in isolated mitochondria, and NAD(+) supplementation restored protein deacetylation and enhanced oxygen consumption in circadian mutant mice. Thus, circadian control of NAD(+) bioavailability modulates mitochondrial oxidative function and organismal metabolism across the daily cycles of fasting and feeding.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3963134/" 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/PMC3963134/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peek, Clara Bien -- Affinati, Alison H -- Ramsey, Kathryn Moynihan -- Kuo, Hsin-Yu -- Yu, Wei -- Sena, Laura A -- Ilkayeva, Olga -- Marcheva, Biliana -- Kobayashi, Yumiko -- Omura, Chiaki -- Levine, Daniel C -- Bacsik, David J -- Gius, David -- Newgard, Christopher B -- Goetzman, Eric -- Chandel, Navdeep S -- Denu, John M -- Mrksich, Milan -- Bass, Joseph -- 5P01HL071643-10/HL/NHLBI NIH HHS/ -- 5P30AR057216-05/AR/NIAMS NIH HHS/ -- F30 DK085936/DK/NIDDK NIH HHS/ -- F30 ES019815/ES/NIEHS NIH HHS/ -- F32 DK092034/DK/NIDDK NIH HHS/ -- P01 AG011412/AG/NIA NIH HHS/ -- P01AG011412-16/AG/NIA NIH HHS/ -- P01DK58398/DK/NIDDK NIH HHS/ -- P30 CA014520/CA/NCI NIH HHS/ -- R01 AG038679/AG/NIA NIH HHS/ -- R01 CA152601-01/CA/NCI NIH HHS/ -- R01 CA152799-01A1/CA/NCI NIH HHS/ -- R01 CA16383801A1/CA/NCI NIH HHS/ -- R01 CA168292/CA/NCI NIH HHS/ -- R01 CA168292-01A1/CA/NCI NIH HHS/ -- R01 DK090242/DK/NIDDK NIH HHS/ -- R01 DK090625/DK/NIDDK NIH HHS/ -- R01 GM065386/GM/NIGMS NIH HHS/ -- R01 HL097817/HL/NHLBI NIH HHS/ -- R01DK090242-03/DK/NIDDK NIH HHS/ -- R01DK090625-01A1/DK/NIDDK NIH HHS/ -- R01HL097817-01/HL/NHLBI NIH HHS/ -- R37 GM059785/GM/NIGMS NIH HHS/ -- T32 DK007169/DK/NIDDK NIH HHS/ -- T32 GM008152/GM/NIGMS NIH HHS/ -- T32 HL007909/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Nov 1;342(6158):1243417. doi: 10.1126/science.1243417. Epub 2013 Sep 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Division of Endocrinology, Metabolism and Molecular Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24051248" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/genetics/metabolism ; Acetylation ; Animals ; Circadian Clocks/genetics/*physiology ; *Energy Metabolism ; Fasting ; Lipid Metabolism ; Liver/metabolism ; Mice ; Mice, Knockout ; Mitochondria, Liver/*metabolism ; NAD/*metabolism ; Oxidation-Reduction ; Oxygen Consumption ; Sirtuin 3/genetics/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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  • 8
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    A novel tumour-suppressor function for the Notch pathway in myeloid leukaemia (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-05-13
    Description: Notch signalling is a central regulator of differentiation in a variety of organisms and tissue types. Its activity is controlled by the multi-subunit gamma-secretase (gammaSE) complex. Although Notch signalling can play both oncogenic and tumour-suppressor roles in solid tumours, in the haematopoietic system it is exclusively oncogenic, notably in T-cell acute lymphoblastic leukaemia, a disease characterized by Notch1-activating mutations. Here we identify novel somatic-inactivating Notch pathway mutations in a fraction of patients with chronic myelomonocytic leukaemia (CMML). Inactivation of Notch signalling in mouse haematopoietic stem cells (HSCs) results in an aberrant accumulation of granulocyte/monocyte progenitors (GMPs), extramedullary haematopoieisis and the induction of CMML-like disease. Transcriptome analysis revealed that Notch signalling regulates an extensive myelomonocytic-specific gene signature, through the direct suppression of gene transcription by the Notch target Hes1. Our studies identify a novel role for Notch signalling during early haematopoietic stem cell differentiation and suggest that the Notch pathway can play both tumour-promoting and -suppressive roles within the same tissue.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3093658/" 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/PMC3093658/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Klinakis, Apostolos -- Lobry, Camille -- Abdel-Wahab, Omar -- Oh, Philmo -- Haeno, Hiroshi -- Buonamici, Silvia -- van De Walle, Inge -- Cathelin, Severine -- Trimarchi, Thomas -- Araldi, Elisa -- Liu, Cynthia -- Ibrahim, Sherif -- Beran, Miroslav -- Zavadil, Jiri -- Efstratiadis, Argiris -- Taghon, Tom -- Michor, Franziska -- Levine, Ross L -- Aifantis, Iannis -- 1P01CA97403/CA/NCI NIH HHS/ -- R01 CA105129/CA/NCI NIH HHS/ -- R01 CA105129-07/CA/NCI NIH HHS/ -- R01 CA133379/CA/NCI NIH HHS/ -- R01 CA133379-04/CA/NCI NIH HHS/ -- R01 CA149655/CA/NCI NIH HHS/ -- R01 CA149655-03/CA/NCI NIH HHS/ -- R01CA105129/CA/NCI NIH HHS/ -- R01CA1328234/CA/NCI NIH HHS/ -- R01CA133379/CA/NCI NIH HHS/ -- R01CA149655/CA/NCI NIH HHS/ -- R21 CA141399/CA/NCI NIH HHS/ -- R21 CA141399-02/CA/NCI NIH HHS/ -- R21CA141399/CA/NCI NIH HHS/ -- U54CA143798/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 May 12;473(7346):230-3. doi: 10.1038/nature09999.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biomedical Research Foundation, Academy of Athens, Athens, Greece.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21562564" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Cell Differentiation ; Cells, Cultured ; Gene Expression Profiling ; *Gene Expression Regulation, Neoplastic ; Gene Silencing ; Genes, Tumor Suppressor/*physiology ; Granulocyte-Macrophage Progenitor Cells/cytology/metabolism ; Hematopoietic Stem Cells/cytology/metabolism ; Homeodomain Proteins/metabolism ; Humans ; Leukemia, Myelomonocytic, Chronic/*genetics/*pathology ; Mice ; Mice, Inbred C57BL ; Mutation ; Receptors, Notch/deficiency/*genetics/*metabolism ; *Signal Transduction ; Tumor Cells, Cultured
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    Image-based genome-wide siRNA screen identifies selective autophagy factors (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-10-25
    Description: Selective autophagy involves the recognition and targeting of specific cargo, such as damaged organelles, misfolded proteins, or invading pathogens for lysosomal destruction. Yeast genetic screens have identified proteins required for different forms of selective autophagy, including cytoplasm-to-vacuole targeting, pexophagy and mitophagy, and mammalian genetic screens have identified proteins required for autophagy regulation. However, there have been no systematic approaches to identify molecular determinants of selective autophagy in mammalian cells. Here, to identify mammalian genes required for selective autophagy, we performed a high-content, image-based, genome-wide small interfering RNA screen to detect genes required for the colocalization of Sindbis virus capsid protein with autophagolysosomes. We identified 141 candidate genes required for viral autophagy, which were enriched for cellular pathways related to messenger RNA processing, interferon signalling, vesicle trafficking, cytoskeletal motor function and metabolism. Ninety-six of these genes were also required for Parkin-mediated mitophagy, indicating that common molecular determinants may be involved in autophagic targeting of viral nucleocapsids and autophagic targeting of damaged mitochondria. Murine embryonic fibroblasts lacking one of these gene products, the C2-domain containing protein, SMURF1, are deficient in the autophagosomal targeting of Sindbis and herpes simplex viruses and in the clearance of damaged mitochondria. Moreover, SMURF1-deficient mice accumulate damaged mitochondria in the heart, brain and liver. Thus, our study identifies candidate determinants of selective autophagy, and defines SMURF1 as a newly recognized mediator of both viral autophagy and mitophagy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3229641/" 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/PMC3229641/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Orvedahl, Anthony -- Sumpter, Rhea Jr -- Xiao, Guanghua -- Ng, Aylwin -- Zou, Zhongju -- Tang, Yi -- Narimatsu, Masahiro -- Gilpin, Christopher -- Sun, Qihua -- Roth, Michael -- Forst, Christian V -- Wrana, Jeffrey L -- Zhang, Ying E -- Luby-Phelps, Katherine -- Xavier, Ramnik J -- Xie, Yang -- Levine, Beth -- AI062773/AI/NIAID NIH HHS/ -- AI109617/AI/NIAID NIH HHS/ -- CA84254/CA/NCI NIH HHS/ -- DK043351/DK/NIDDK NIH HHS/ -- DK086502/DK/NIDDK NIH HHS/ -- DK83756/DK/NIDDK NIH HHS/ -- P30 DK040561/DK/NIDDK NIH HHS/ -- P30 DK040561-15/DK/NIDDK NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- R01 AI051367/AI/NIAID NIH HHS/ -- R01 AI051367-06/AI/NIAID NIH HHS/ -- UL1 RR024982/RR/NCRR NIH HHS/ -- ZIA BC011168-03/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Dec 1;480(7375):113-7. doi: 10.1038/nature10546.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9113, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22020285" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy/*genetics ; Capsid Proteins/metabolism ; *Genome-Wide Association Study ; HeLa Cells ; Humans ; Lysosomes/metabolism ; Mice ; Mitochondria/metabolism ; Protein Transport/genetics ; RNA, Small Interfering/*genetics ; Sindbis Virus/metabolism ; Ubiquitin-Protein Ligases/deficiency/genetics
    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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    Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-01-20
    Description: Exercise has beneficial effects on human health, including protection against metabolic disorders such as diabetes. However, the cellular mechanisms underlying these effects are incompletely understood. The lysosomal degradation pathway, autophagy, is an intracellular recycling system that functions during basal conditions in organelle and protein quality control. During stress, increased levels of autophagy permit cells to adapt to changing nutritional and energy demands through protein catabolism. Moreover, in animal models, autophagy protects against diseases such as cancer, neurodegenerative disorders, infections, inflammatory diseases, ageing and insulin resistance. Here we show that acute exercise induces autophagy in skeletal and cardiac muscle of fed mice. To investigate the role of exercise-mediated autophagy in vivo, we generated mutant mice that show normal levels of basal autophagy but are deficient in stimulus (exercise- or starvation)-induced autophagy. These mice (termed BCL2 AAA mice) contain knock-in mutations in BCL2 phosphorylation sites (Thr69Ala, Ser70Ala and Ser84Ala) that prevent stimulus-induced disruption of the BCL2-beclin-1 complex and autophagy activation. BCL2 AAA mice show decreased endurance and altered glucose metabolism during acute exercise, as well as impaired chronic exercise-mediated protection against high-fat-diet-induced glucose intolerance. Thus, exercise induces autophagy, BCL2 is a crucial regulator of exercise- (and starvation)-induced autophagy in vivo, and autophagy induction may contribute to the beneficial metabolic effects of exercise.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518436/" 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/PMC3518436/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Congcong -- Bassik, Michael C -- Moresi, Viviana -- Sun, Kai -- Wei, Yongjie -- Zou, Zhongju -- An, Zhenyi -- Loh, Joy -- Fisher, Jill -- Sun, Qihua -- Korsmeyer, Stanley -- Packer, Milton -- May, Herman I -- Hill, Joseph A -- Virgin, Herbert W -- Gilpin, Christopher -- Xiao, Guanghua -- Bassel-Duby, Rhonda -- Scherer, Philipp E -- Levine, Beth -- 1P01 DK0887761/DK/NIDDK NIH HHS/ -- P01 DK088761/DK/NIDDK NIH HHS/ -- P30 CA142543/CA/NCI NIH HHS/ -- R01 CA109618/CA/NCI NIH HHS/ -- R01 CA112023/CA/NCI NIH HHS/ -- R01 DK055758/DK/NIDDK NIH HHS/ -- R0I AI084887/AI/NIAID NIH HHS/ -- R0I HL080244/HL/NHLBI NIH HHS/ -- R0I HL090842/HL/NHLBI NIH HHS/ -- RC1 DK086629/DK/NIDDK NIH HHS/ -- RCI DK086629/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Jan 18;481(7382):511-5. doi: 10.1038/nature10758.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Autophagy Research, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22258505" target="_blank"〉PubMed〈/a〉
    Keywords: Adiponectin/blood ; Animals ; Apoptosis Regulatory Proteins/genetics/metabolism ; Autophagy/drug effects/genetics/*physiology ; Cells, Cultured ; Dietary Fats/adverse effects ; Food Deprivation/physiology ; Gene Knock-In Techniques ; Glucose/*metabolism ; Glucose Intolerance/chemically induced/prevention & control ; Glucose Tolerance Test ; *Homeostasis/drug effects ; Leptin/blood ; Male ; Mice ; Mice, Transgenic ; Muscle, Skeletal/cytology/drug effects/*metabolism ; Mutation ; Myocardium/cytology/*metabolism ; Phosphorylation/genetics ; Physical Conditioning, Animal/*physiology ; Physical Endurance/genetics/physiology ; Physical Exertion/genetics/physiology ; Protein Binding/genetics ; Proto-Oncogene Proteins/genetics/*metabolism ; Proto-Oncogene Proteins c-bcl-2 ; Running/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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