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  • Cell Research
    de Duve s coining of the term autophagy for the degradation process of cytoplasmic constituents in the lysosome vacuole This year we regretfully lost this great scientist who contributed much during the early years of research to the field of autophagy Soon after the discovery of lysosomes by de Duve electron microscopy revealed autophagy as a means of delivering intracellular components to the lysosome For a long time after the discovery of autophagy studies failed to yield any significant advances at a molecular level in our understanding of this fundamental pathway of degradation The first breakthrough was made in the early 1990s as autophagy was discovered in yeast subjected to starvation by microscopic observation Next a genetic effort to address the poorly understood problem of autophagy led to the discovery of many autophagy defective mutants Subsequent identification of autophagy related genes in yeast revealed unique sets of molecules involved in membrane dynamics during autophagy ATG homologs were subsequently found in various organisms indicating that the fundamental mechanism of autophagy is well conserved among eukaryotes These findings brought revolutionary changes to research in this field For instance the last 10 years have seen remarkable progress in our understanding of autophagy not

    Original URL path: http://www.cell-research.com/arts.asp?id=1866 (2016-02-14)
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  • Cell Research
    Autophagy is a primarily degradative pathway that takes place in all eukaryotic cells It is used for recycling cytoplasm to generate macromolecular building blocks and energy under stress conditions to remove superfluous and damaged organelles to adapt to changing nutrient conditions and to maintain cellular homeostasis In addition autophagy plays a critical role in cytoprotection by preventing the accumulation of toxic proteins and through its action in various aspects of immunity including the elimination of invasive microbes and its participation in antigen presentation The most prevalent form of autophagy is macroautophagy and during this process the cell forms a double membrane sequestering compartment termed the phagophore which matures into an autophagosome Following delivery to the vacuole or lysosome the cargo is degraded and the resulting macromolecules are released back into the cytosol for reuse The past two decades have resulted in a tremendous increase with regard to the molecular studies of autophagy being carried out in yeast and other eukaryotes Part of the surge in interest in this topic is due to the connection of autophagy with a wide range of human pathophysiologies including cancer myopathies diabetes and neurodegenerative disease However there are still many aspects of autophagy that remain

    Original URL path: http://www.cell-research.com/arts.asp?id=1867 (2016-02-14)
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  • Cell Research
    Autophagy regulation by nutrient signaling FREE Ryan C Russell 1 Hai Xin Yuan 1 and Kun Liang Guan 1 1 Department of Pharmacology and Moores Cancer Center University of California San Diego La Jolla CA 92093 0815 USA Correspondence Kun Liang Guan E mail kuguan ucsd edu The ability of cells to respond to changes in nutrient availability is essential for the maintenance of metabolic homeostasis and viability One of the key cellular responses to nutrient withdrawal is the upregulation of autophagy Recently there has been a rapid expansion in our knowledge of the molecular mechanisms involved in the regulation of mammalian autophagy induction in response to depletion of key nutrients Intracellular amino acids ATP and oxygen levels are intimately tied to the cellular balance of anabolic and catabolic processes Signaling from key nutrient sensitive kinases mTORC1 and AMP activated protein kinase AMPK is essential for the nutrient sensing of the autophagy pathway Recent advances have shown that the nutrient status of the cell is largely passed on to the autophagic machinery through the coordinated regulation of the ULK and VPS34 kinase complexes Identification of extensive crosstalk and feedback loops converging on the regulation of ULK and VPS34 can be

    Original URL path: http://www.cell-research.com/arts.asp?id=1868 (2016-02-14)
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  • Cell Research
    Submission Advanced Online Publication Current Issue Top 10 VOLUME 24 ISSUE 1 1 2014 58 68 A current perspective of autophagosome biogenesis FREE Shusaku T Shibutani 1 2 and Tamotsu Yoshimori 1 2 1 Laboratory of Intracellular Membrane Dynamics Graduate School of Frontier Biosciences Osaka University Osaka 565 0871 Japan 2 Department of Genetics Graduate School of Medicine Osaka University Osaka 565 0871 Japan Correspondence Tamotsu Yoshimori Tel 81 6 6879 3580 Fax 81 6 6879 3589 E mail tamyoshi fbs osaka u ac jp Autophagy is a bulk degradation system induced by cellular stresses such as nutrient starvation Its function relies on the formation of double membrane vesicles called autophagosomes Unlike other organelles that appear to stably exist in the cell autophagosomes are formed on demand and once their formation is initiated it proceeds surprisingly rapidly How and where this dynamic autophagosome formation takes place has been a long standing question but the discovery of Atg proteins in the 1990 s significantly accelerated our understanding of autophagosome biogenesis In this review we will briefly introduce each Atg functional unit in relation to autophagosome biogenesis and then discuss the origin of the autophagosomal membrane with an introduction to selected recent

    Original URL path: http://www.cell-research.com/arts.asp?id=1869 (2016-02-14)
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  • Cell Research
    VOLUME 24 ISSUE 1 1 2014 69 79 Autophagy and human diseases FREE Peidu Jiang 1 2 and Noboru Mizushima 1 2 1 Department of Biochemistry and Molecular Biology Graduate School and Faculty of Medicine The University of Tokyo Tokyo 113 0033 Japan 2 Department of Physiology and Cell Biology Tokyo Medical and Dental University Tokyo 113 8519 Japan Correspondence Noboru Mizushima Tel 81 3 5841 3440 Fax 81 3 3815 1490 E mail nmizu m u tokyo ac jp Autophagy is a major intracellular degradative process that delivers cytoplasmic materials to the lysosome for degradation Since the discovery of autophagy related Atg genes in the 1990s there has been a proliferation of studies on the physiological and pathological roles of autophagy in a variety of autophagy knockout models However direct evidence of the connections between ATG gene dysfunction and human diseases has emerged only recently There are an increasing number of reports showing that mutations in the ATG genes were identified in various human diseases such as neurodegenerative diseases infectious diseases and cancers Here we review the major advances in identification of mutations or polymorphisms of the ATG genes in human diseases Current autophagy modulating compounds in clinical trials

    Original URL path: http://www.cell-research.com/arts.asp?id=1945 (2016-02-14)
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  • Cell Research
    during C elegans development FREE Peiguo Yang 1 and Hong Zhang 1 1 State Key Laboratory of Biomacromolecules Institute of Biophysics Chinese Academy of Sciences 15 Datun Road Chaoyang District Beijing 100101 China Correspondence Hong Zhang Tel 86 10 64848238 Fax 86 10 64853925 E mail hongzhang sun5 ibp ac cn Autophagy involves the sequestration of a portion of the cytosolic contents in an enclosed double membrane autophagosomal structure and its subsequent delivery to lysosomes for degradation Autophagy activity functions in multiple biological processes during Caenorhabditis elegans development The basal level of autophagy in embryos removes aggregate prone proteins paternal mitochondria and spermatid specific membranous organelles MOs Autophagy also contributes to the efficient removal of embryonic apoptotic cell corpses by promoting phagosome maturation During larval development autophagy modulates miRNA mediated gene silencing by selectively degrading AIN 1 a component of miRNA induced silencing complex and thus participates in the specification of multiple cell fates controlled by miRNAs During development of the hermaphrodite germline autophagy acts coordinately with the core apoptotic machinery to execute genotoxic stress induced germline cell death and also cell death when caspase activity is partially compromised Autophagy is also involved in the utilization of lipid droplets in

    Original URL path: http://www.cell-research.com/arts.asp?id=1870 (2016-02-14)
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  • Cell Research
    roles in disease and aging FREE Ana Maria Cuervo 1 and Esther Wong 2 1 Department of Developmental and Molecular Biology Institute for Aging Studies Marion Bessin Liver Research Center Albert Einstein College of Medicine 1300 Morris Park Avenue Chanin Building 504 Bronx NY 10461 USA 2 School of Biological Sciences Nanyang Technological University SBS 03n 05 60 Nanyang Drive Singapore 637551 Singapore Correspondence Esther Wong Tel 65 6316 2848 Fax 65 6791 3856 E mail EstherWong ntu edu sg This review focuses on chaperone mediated autophagy CMA one of the proteolytic systems that contributes to degradation of intracellular proteins in lysosomes CMA substrate proteins are selectively targeted to lysosomes and translocated into the lysosomal lumen through the coordinated action of chaperones located at both sides of the membrane and a dedicated protein translocation complex The selectivity of CMA permits timed degradation of specific proteins with regulatory purposes supporting a modulatory role for CMA in enzymatic metabolic processes and subsets of the cellular transcriptional program In addition CMA contributes to cellular quality control through the removal of damaged or malfunctioning proteins Here we describe recent advances in the understanding of the molecular dynamics regulation and physiology of CMA and discuss

    Original URL path: http://www.cell-research.com/arts.asp?id=1871 (2016-02-14)
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  • Cell Research
    University Xiamen Fujian 361005 China Correspondence Jiahuai Han E mail jhan xmu edu cn E mail jhan scripps edu Mixed lineage kinase domain like protein MLKL was identified to function downstream of receptor interacting protein 3 RIP3 in tumor necrosis factor α TNF induced necrosis also called necroptosis However how MLKL functions to mediate necroptosis is unknown By reconstitution of MLKL function in MLKL knockout cells we showed that the N terminus of MLKL is required for its function in necroptosis The oligomerization of MLKL in TNF treated cells is essential for necroptosis as artificially forcing MLKL together by using the hormone binding domain HBD triggers necroptosis Notably forcing together the N terminal domain ND but not the C terminal kinase domain of MLKL causes necroptosis Further deletion analysis showed that the four α helix bundle of MLKL 1 130 amino acids is sufficient to trigger necroptosis Both the HBD mediated and TNF induced complexes of MLKL ND or MLKL are tetramers and translocation of these complexes to lipid rafts of the plasma membrane precedes cell death The homo oligomerization is required for MLKL translocation and the signal sequence for plasma membrane location is located in the junction of the

    Original URL path: http://www.cell-research.com/arts.asp?id=1872 (2016-02-14)
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