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  • 1
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    Is SIRT2 required for necroptosis? (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-02-28
    Description: Sirtuins can promote deacetylation of a wide range of substrates in diverse cellular compartments and regulate many cellular processes(1),(2). Recently Narayan et al., reported that SIRT2 was required for necroptosis based on their findings that SIRT2 inhibition, knock-down or knock-out prevented necroptosis. We sought to confirm and explore the role of SIRT2 in necroptosis and tested four different sources of the SIRT2 inhibitor AGK2, three independent siRNAs against SIRT2, and cells from two independently generated Sirt2-/- mouse strains, however we were unable to show that inhibiting or depleting SIRT2 protected cells from necroptosis. Furthermore, Sirt2-/- mice succumbed to TNF induced Systemic Inflammatory Response Syndrome (SIRS) more rapidly than wild type mice while Ripk3-/- mice were resistant. Our results therefore question the importance of SIRT2 in the necroptosis cell death pathway.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4005920/" 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/PMC4005920/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Newton, Kim -- Hildebrand, Joanne M -- Shen, Zhirong -- Rodriguez, Diego -- Alvarez-Diaz, Silvia -- Petersen, Sean -- Shah, Saumil -- Dugger, Debra L -- Huang, Chunzi -- Auwerx, Johan -- Vandenabeele, Peter -- Green, Douglas R -- Ashkenazi, Avi -- Dixit, Vishva M -- Kaiser, William J -- Strasser, Andreas -- Degterev, Alexei -- Silke, John -- P30 CA021765/CA/NCI NIH HHS/ -- R01 AI044828/AI/NIAID NIH HHS/ -- R01 CA169291/CA/NCI NIH HHS/ -- England -- Nature. 2014 Feb 27;506(7489):E4-6. doi: 10.1038/nature13024.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genentech, Inc., South San Francisco, California 94080, USA. ; 1] The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia [2] Department of Medical Biology, University of Melbourne, Parkville, Victoria 3050, Australia. ; National Institute of Biological Sciences, Zhongguancun Life Science Park, Beijing 102206, China. ; Department of Immunology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; Department of Biochemistry, Tufts University, Boston, Massachusetts 02111, USA. ; Department of Microbiology and Immunology, Emory Vaccine Center, Emory University School of Medicine, Atlanta, Georgia 30322, USA. ; Laboratory of Integrative and Systems Physiology, EPFL, CH-1015 Lausanne, Switzerland. ; 1] Molecular Signaling and Cell Death Unit, Inflammation Research Center, VIB, 9052 Gent, Belgium [2] Department of Biomedical Molecular Biology, Ghent University, 9052 Gent, Belgium [3] Methusalem BOF09/01M00709, Ghent University, 9052 Gent, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24572428" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Humans ; Male ; Necrosis/*enzymology ; Sirtuin 2/*genetics/*metabolism
    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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    Catalytic activity of the caspase-8-FLIP(L) complex inhibits RIPK3-dependent necrosis (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-03-04
    Description: Caspase-8 has two opposing biological functions--it promotes cell death by triggering the extrinsic pathway of apoptosis, but also has a survival activity, as it is required for embryonic development, T-lymphocyte activation, and resistance to necrosis induced by tumour necrosis factor-alpha (TNF-alpha) and related family ligands. Here we show that development of caspase-8-deficient mice is completely rescued by ablation of receptor interacting protein kinase-3 (RIPK3). Adult animals lacking both caspase-8 and RIPK3 display a progressive lymphoaccumulative disease resembling that seen with defects in CD95 or CD95-ligand (also known as FAS and FASLG, respectively), and resist the lethal effects of CD95 ligation in vivo. We have found that caspase-8 prevents RIPK3-dependent necrosis without inducing apoptosis by functioning in a proteolytically active complex with FLICE-like inhibitory protein long (FLIP(L), also known as CFLAR), and this complex is required for the protective function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3077893/" 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/PMC3077893/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oberst, Andrew -- Dillon, Christopher P -- Weinlich, Ricardo -- McCormick, Laura L -- Fitzgerald, Patrick -- Pop, Cristina -- Hakem, Razq -- Salvesen, Guy S -- Green, Douglas R -- P01 CA069381/CA/NCI NIH HHS/ -- P01 CA069381-14/CA/NCI NIH HHS/ -- England -- Nature. 2011 Mar 17;471(7338):363-7. doi: 10.1038/nature09852. Epub 2011 Mar 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dept. of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21368763" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/deficiency/metabolism ; Apoptosis ; *Biocatalysis ; CASP8 and FADD-Like Apoptosis Regulating Protein/*metabolism ; Caspase 8/genetics/*metabolism ; Caspase Inhibitors ; Cell Line ; Female ; Male ; Mice ; Multiprotein Complexes/chemistry/metabolism ; *Necrosis ; Phenotype ; Receptor-Interacting Protein Serine-Threonine Kinases/*antagonists & ; inhibitors/deficiency/genetics/*metabolism ; Serpins/pharmacology ; Tumor Necrosis Factor-alpha/antagonists & inhibitors/biosynthesis/pharmacology ; Viral Proteins/pharmacology
    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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  • 3
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    Metabolic maintenance of cell asymmetry following division in activated T lymphocytes (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-04-12
    Description: Asymmetric cell division, the partitioning of cellular components in response to polarizing cues during mitosis, has roles in differentiation and development. It is important for the self-renewal of fertilized zygotes in Caenorhabditis elegans and neuroblasts in Drosophila, and in the development of mammalian nervous and digestive systems. T lymphocytes, upon activation by antigen-presenting cells (APCs), can undergo asymmetric cell division, wherein the daughter cell proximal to the APC is more likely to differentiate into an effector-like T cell and the distal daughter is more likely to differentiate into a memory-like T cell. Upon activation and before cell division, expression of the transcription factor c-Myc drives metabolic reprogramming, necessary for the subsequent proliferative burst. Here we find that during the first division of an activated T cell in mice, c-Myc can sort asymmetrically. Asymmetric distribution of amino acid transporters, amino acid content, and activity of mammalian target of rapamycin complex 1 (mTORC1) is correlated with c-Myc expression, and both amino acids and mTORC1 activity sustain the differences in c-Myc expression in one daughter cell compared to the other. Asymmetric c-Myc levels in daughter T cells affect proliferation, metabolism, and differentiation, and these effects are altered by experimental manipulation of mTORC1 activity or c-Myc expression. Therefore, metabolic signalling pathways cooperate with transcription programs to maintain differential cell fates following asymmetric T-cell division.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4851250/" 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/PMC4851250/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Verbist, Katherine C -- Guy, Cliff S -- Milasta, Sandra -- Liedmann, Swantje -- Kaminski, Marcin M -- Wang, Ruoning -- Green, Douglas R -- R01 GM096208/GM/NIGMS NIH HHS/ -- R37 GM052735/GM/NIGMS NIH HHS/ -- England -- Nature. 2016 Apr 21;532(7599):389-93. doi: 10.1038/nature17442. Epub 2016 Apr 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, Tennessee 38105, USA. ; Center for Childhood Cancer and Blood Disease, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio 43205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27064903" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Transport Systems/metabolism ; Amino Acids/metabolism ; Animals ; CD8-Positive T-Lymphocytes/*cytology/*metabolism ; Cell Differentiation/genetics ; *Cell Division ; *Cell Polarity/genetics ; Female ; *Lymphocyte Activation ; Male ; Mice ; Multiprotein Complexes/metabolism ; Proto-Oncogene Proteins c-myc/genetics/metabolism ; Signal Transduction/genetics ; TOR Serine-Threonine Kinases/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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  • 4
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    Noncanonical autophagy inhibits the autoinflammatory, lupus-like response to dying cells (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-04-21
    Description: Defects in clearance of dying cells have been proposed to underlie the pathogenesis of systemic lupus erythematosus (SLE). Mice lacking molecules associated with dying cell clearance develop SLE-like disease, and phagocytes from patients with SLE often display defective clearance and increased inflammatory cytokine production when exposed to dying cells in vitro. Previously, we and others described a form of noncanonical autophagy known as LC3-associated phagocytosis (LAP), in which phagosomes containing engulfed particles, including dying cells, recruit elements of the autophagy pathway to facilitate maturation of phagosomes and digestion of their contents. Genome-wide association studies have identified polymorphisms in the Atg5 (ref. 8) and possibly Atg7 (ref. 9) genes, involved in both canonical autophagy and LAP, as markers of a predisposition for SLE. Here we describe the consequences of defective LAP in vivo. Mice lacking any of several components of the LAP pathway show increased serum levels of inflammatory cytokines and autoantibodies, glomerular immune complex deposition, and evidence of kidney damage. When dying cells are injected into LAP-deficient mice, they are engulfed but not efficiently degraded and trigger acute elevation of pro-inflammatory cytokines but not anti-inflammatory interleukin (IL)-10. Repeated injection of dying cells into LAP-deficient, but not LAP-sufficient, mice accelerated the development of SLE-like disease, including increased serum levels of autoantibodies. By contrast, mice deficient in genes required for canonical autophagy but not LAP do not display defective dying cell clearance, inflammatory cytokine production, or SLE-like disease, and, like wild-type mice, produce IL-10 in response to dying cells. Therefore, defects in LAP, rather than canonical autophagy, can cause SLE-like phenomena, and may contribute to the pathogenesis of SLE.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4860026/" 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/PMC4860026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martinez, Jennifer -- Cunha, Larissa D -- Park, Sunmin -- Yang, Mao -- Lu, Qun -- Orchard, Robert -- Li, Quan-Zhen -- Yan, Mei -- Janke, Laura -- Guy, Cliff -- Linkermann, Andreas -- Virgin, Herbert W -- Green, Douglas R -- 1ZIAES10328601/PHS HHS/ -- R01 AI040646/AI/NIAID NIH HHS/ -- R01 AI40646/AI/NIAID NIH HHS/ -- U19 AI109725/AI/NIAID NIH HHS/ -- ZIA ES103286-01/Intramural NIH HHS/ -- England -- Nature. 2016 May 5;533(7601):115-9. doi: 10.1038/nature17950. Epub 2016 Apr 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; Immunity, Inflammation, and Disease Laboratory, National Institute of Environmental Health Sciences, 111 T.W. Alexander Drive, Research Triangle Park, North Carolina 27709, USA. ; Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; Division of Nephrology and Hypertension, Christian-Albrechts-University, Kiel 24105, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27096368" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Antibody Complex/metabolism ; Autoantibodies/blood ; *Autophagy/genetics ; Cytokines/biosynthesis/blood ; Inflammation/blood/genetics/*pathology ; Interleukin-10/biosynthesis ; Kidney/metabolism/pathology ; Lupus Erythematosus, Systemic/blood/genetics/*immunology/*pathology ; Male ; Mice ; Microtubule-Associated Proteins/metabolism ; Phagocytes/cytology/physiology ; Phagosomes/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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