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  1. Article ; Online: Autophagy and the evasion of host defense: a new variation on the theme for Burkholderia cepacia?

    Devenish, Rodney J

    Autophagy

    2011  Volume 7, Issue 11, Page(s) 1269–1270

    MeSH term(s) Animals ; Autophagy/drug effects ; Burkholderia Infections/drug therapy ; Burkholderia cenocepacia/physiology ; Cystic Fibrosis/drug therapy ; Pneumonia/drug therapy ; Sirolimus/pharmacology ; Sirolimus/therapeutic use
    Chemical Substances Sirolimus (W36ZG6FT64)
    Language English
    Publishing date 2011-11
    Publishing country United States
    Document type Comment ; Editorial
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.4161/auto.7.11.17941
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  2. Article ; Online: Autophagy: starvation relieves transcriptional repression of ATG genes.

    Devenish, Rodney J / Prescott, Mark

    Current biology : CB

    2015  Volume 25, Issue 6, Page(s) R238–40

    Abstract: Autophagy is a highly regulated process about which relatively little is known, particularly concerning the transcriptional control of autophagy regulation. A new study identifies a key regulator of the expression of autophagy-related genes, thereby ... ...

    Abstract Autophagy is a highly regulated process about which relatively little is known, particularly concerning the transcriptional control of autophagy regulation. A new study identifies a key regulator of the expression of autophagy-related genes, thereby providing insights into the signalling pathways modulating autophagy.
    MeSH term(s) Autophagy/genetics ; Autophagy/physiology ; Genes, Fungal ; Histone Demethylases/genetics ; Histone Demethylases/physiology ; Mutation ; Protein Kinases/genetics ; Protein Kinases/physiology ; Repressor Proteins/genetics ; Repressor Proteins/physiology ; Saccharomyces cerevisiae/cytology ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae/physiology ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/physiology ; Signal Transduction/genetics ; Signal Transduction/physiology ; Transcription, Genetic
    Chemical Substances RPH1 protein, S cerevisiae ; Repressor Proteins ; Saccharomyces cerevisiae Proteins ; Histone Demethylases (EC 1.14.11.-) ; Protein Kinases (EC 2.7.-) ; Rim15 protein, S cerevisiae (EC 2.7.1.-)
    Language English
    Publishing date 2015-03-16
    Publishing country England
    Document type Journal Article
    ZDB-ID 1071731-6
    ISSN 1879-0445 ; 0960-9822
    ISSN (online) 1879-0445
    ISSN 0960-9822
    DOI 10.1016/j.cub.2015.01.045
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  3. Article: Mitophagy: growing in intricacy.

    Devenish, Rodney J

    Autophagy

    2007  Volume 3, Issue 4, Page(s) 293–294

    MeSH term(s) Autophagy/physiology ; Gene Deletion ; Gene Expression Regulation, Fungal ; Gene Silencing ; Genes, Mitochondrial ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondria/physiology ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae/metabolism
    Language English
    Publishing date 2007-07-13
    Publishing country United States
    Document type Comment ; Editorial
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.4161/auto.4273
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  4. Article ; Online: Autophagy and burkholderia.

    Devenish, Rodney J / Lai, Shu-chin

    Immunology and cell biology

    2014  Volume 93, Issue 1, Page(s) 18–24

    Abstract: Autophagy has become increasingly viewed as an important component of the eukaryotic innate immune system. The elimination of intracellular pathogens by autophagy in mammalian cells (xenophagy) results not only in the degradation of invading bacteria, ... ...

    Abstract Autophagy has become increasingly viewed as an important component of the eukaryotic innate immune system. The elimination of intracellular pathogens by autophagy in mammalian cells (xenophagy) results not only in the degradation of invading bacteria, viruses, fungi and parasites, but also liberation of metabolites that may have been utilized during pathogen infection, thus promoting cell survival. After gaining entry into the cell, intracellular bacterial pathogens attempt to escape from phagosomes (or endosomes) into the cytosol where they endeavour to continue the infection cycle unhindered by host cell protective mechanisms. Bacterial recognition resulting from either their cytosolic location, the secretion of bacterial products, or phagosomal membrane damage, can induce autophagy. In this context, induction of autophagy results in the clearance of some bacterial pathogens, whereas other bacteria are able to manipulate autophagy for their own benefit and appear to effectively replicate within autophagosome-like vesicles. Some bacteria are seemingly able to evade autophagy and Burkholderia pseudomallei is one of them. This review will discuss the autophagic processes that may be activated by host cells to provide protection against infection by this bacterial pathogen.
    MeSH term(s) Autophagy/genetics ; Autophagy/immunology ; Bacterial Proteins/genetics ; Bacterial Proteins/immunology ; Burkholderia pseudomallei/immunology ; Gene Expression Regulation ; Host-Pathogen Interactions ; Humans ; Immune Evasion ; Immunity, Innate ; Macrophages/immunology ; Macrophages/microbiology ; Macrophages/pathology ; Melioidosis/genetics ; Melioidosis/immunology ; Melioidosis/microbiology ; Melioidosis/pathology ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/immunology ; Phagosomes/chemistry ; Phagosomes/genetics ; Phagosomes/immunology ; Signal Transduction ; Ubiquitin/genetics ; Ubiquitin/immunology
    Chemical Substances Bacterial Proteins ; MAP1LC3A protein, human ; Microtubule-Associated Proteins ; Ubiquitin
    Language English
    Publishing date 2014-10-21
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 284057-1
    ISSN 1440-1711 ; 0818-9641
    ISSN (online) 1440-1711
    ISSN 0818-9641
    DOI 10.1038/icb.2014.87
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  5. Article ; Online: Nucleophagy at a glance.

    Mijaljica, Dalibor / Devenish, Rodney J

    Journal of cell science

    2013  Volume 126, Issue Pt 19, Page(s) 4325–4330

    Abstract: Under certain circumstances, the removal of damaged or non-essential parts of the nucleus, or even an entire nucleus, is crucial in order to promote cell longevity and enable proper function. A selective form of autophagy, known as nucleophagy, can be ... ...

    Abstract Under certain circumstances, the removal of damaged or non-essential parts of the nucleus, or even an entire nucleus, is crucial in order to promote cell longevity and enable proper function. A selective form of autophagy, known as nucleophagy, can be used to accomplish the degradation of nucleus-derived material. In this Cell Science at a Glance article and the accompanying poster, we summarize the similarities and differences between the divergent modes of nucleophagy that have been described to date, emphasizing, where possible, the molecular mechanism, the membrane interactions and rearrangements, and the nature of the nucleus-derived material that is degraded. In turn, we will consider nucleophagy processes in the lower eukaryotes, the budding yeast Saccharomyces cerevisiae, filamentous fungi Aspergillus and Magnaporthe oryzae and the ciliated protozoan Tetrahymena thermophila, and finally in mammalian cells. We will also briefly discuss the emerging links between nucleophagy and human disease.
    MeSH term(s) Animals ; Autophagy/physiology ; Cell Nucleus/physiology ; Humans
    Language English
    Publishing date 2013-10-01
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2993-2
    ISSN 1477-9137 ; 0021-9533
    ISSN (online) 1477-9137
    ISSN 0021-9533
    DOI 10.1242/jcs.133090
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  6. Article ; Online: Autophagy: mechanism and physiological relevance 'brewed' from yeast studies.

    Devenish, Rodney J / Klionsky, Daniel J

    Frontiers in bioscience (Scholar edition)

    2012  Volume 4, Issue 4, Page(s) 1354–1363

    Abstract: Autophagy is a highly conserved process of quality control occurring inside cells by which cytoplasmic material can be degraded and the products recycled for use as new building blocks or for energy production. The rapid progress and 'explosion' of ... ...

    Abstract Autophagy is a highly conserved process of quality control occurring inside cells by which cytoplasmic material can be degraded and the products recycled for use as new building blocks or for energy production. The rapid progress and 'explosion' of knowledge concerning autophagic processes in mammals/humans that has occurred over the last 15 years was driven by fundamental studies in yeast, principally using Saccharomyces cerevisiae, leading to the identification and cloning of genes required for autophagy. This chapter reviews the role of yeast studies in understanding the molecular mechanisms of autophagic processes, focusing on aspects that are conserved in mammals/humans and how autophagy is increasingly implicated in the pathogenesis of disease and is required for development and differentiation.
    MeSH term(s) Animals ; Autophagy/genetics ; Autophagy/physiology ; Humans ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae/metabolism ; Saccharomyces cerevisiae/physiology
    Language English
    Publishing date 2012-06-01
    Publishing country Singapore
    Document type Journal Article ; Review
    ZDB-ID 2565100-6
    ISSN 1945-0524 ; 1945-0516
    ISSN (online) 1945-0524
    ISSN 1945-0516
    DOI 10.2741/s337
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  7. Article: LC3-Associated Phagocytosis (LAP): Connections with Host Autophagy.

    Lai, Shu-Chin / Devenish, Rodney J

    Cells

    2012  Volume 1, Issue 3, Page(s) 396–408

    Abstract: Autophagy is an intracellular degradative process with a number of roles, one of which can be the protection of eukaryotic cells from invading microbes. Microtubule-associated protein light-chain 3 (LC3) is a key autophagy-related protein that is ... ...

    Abstract Autophagy is an intracellular degradative process with a number of roles, one of which can be the protection of eukaryotic cells from invading microbes. Microtubule-associated protein light-chain 3 (LC3) is a key autophagy-related protein that is recruited to the double-membrane autophagosome responsible for sequestering material intended for delivery to lysosomes. GFP-LC3 is widely used as a marker of autophagosome formation as denoted by the formation of green puncta when viewed by fluorescence microscopy. Recently, it has been demonstrated that LC3 can be recruited to other membranes including single-membrane phagosomes, in a process termed LC3-associated phagocytosis (LAP). Thus, the observation of green puncta in cells can no longer, by itself, be taken as evidence of autophagy. This review will clarify those features of LAP which serve to distinguish it from autophagy and that make connections with host autophagic responses in terms of infection by microbial pathogens. More specifically, it will refer to concurrent studies of the mechanism by which LAP is triggered in comparison to autophagy.
    Language English
    Publishing date 2012-07-30
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2661518-6
    ISSN 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells1030396
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  8. Article ; Online: A conference report from "Down Under": Talking autophagy at OzBio2010.

    Mijaljica, Dalibor / Devenish, Rodney J

    Autophagy

    2011  Volume 7, Issue 2, Page(s) 252–254

    Abstract: OzBio2010 was held at the Melbourne Convention and Exhibition Centre, September 26 to October 1, 2010. This international conference catered to researchers in several fields having complementary interests including biochemistry, molecular biology, cell ... ...

    Abstract OzBio2010 was held at the Melbourne Convention and Exhibition Centre, September 26 to October 1, 2010. This international conference catered to researchers in several fields having complementary interests including biochemistry, molecular biology, cell biology, plant physiology and health-related research. It was held under the auspices of two major international scientific societies, IUBMB and FAOBMB, and the ComBio2010 collective (representing nine professional societies and groupings from Australia). A number of pre-eminent speakers presented at plenary sessions and in a wide array of specialist symposia. One of the plenary sessions and a specialist symposium highlighted autophagy-related topics.
    MeSH term(s) Animals ; Australia ; Autophagy ; Burkholderia pseudomallei/physiology ; Drosophila melanogaster/genetics ; Humans ; Macrophages/microbiology ; Mice ; Mitochondria/metabolism ; Mutation/genetics ; Protein Kinases/metabolism ; Protein Transport ; RNA Processing, Post-Transcriptional ; RNA, Ribosomal/metabolism ; Signal Transduction ; Ubiquitin-Protein Ligases/metabolism ; Zebrafish/genetics
    Chemical Substances RNA, Ribosomal ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; parkin protein (EC 2.3.2.27) ; Protein Kinases (EC 2.7.-) ; PTEN-induced putative kinase (EC 2.7.11.1)
    Language English
    Publishing date 2011-02-01
    Publishing country United States
    Document type Congress
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.4161/auto.7.2.14225
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  9. Article ; Online: Inhibition of bioenergetics provides novel insights into recruitment of PINK1-dependent neuronal mitophagy.

    Shin, Yea Seul / Ryall, James G / Britto, Joanne M / Lau, Chew L / Devenish, Rodney J / Nagley, Phillip / Beart, Philip M

    Journal of neurochemistry

    2019  Volume 149, Issue 2, Page(s) 269–283

    Abstract: Contributions of damaged mitochondria to neuropathologies have stimulated interest in mitophagy. We investigated triggers of neuronal mitophagy by disruption of mitochondrial energy metabolism in primary neurons. Mitophagy was examined in cultured murine ...

    Abstract Contributions of damaged mitochondria to neuropathologies have stimulated interest in mitophagy. We investigated triggers of neuronal mitophagy by disruption of mitochondrial energy metabolism in primary neurons. Mitophagy was examined in cultured murine cerebellar granule cells after inhibition of mitochondrial respiratory chain by drugs rotenone, 3-nitropropionic acid, antimycin A, and potassium cyanide, targeting complexes I, II, III, and IV, respectively. Inhibitor concentrations producing slow cellular demise were determined from analyses of cellular viability, morphology of neuritic damage, plasma membrane permeability, and oxidative phosphorylation. Live cell imaging of dissipation of mitochondrial membrane potential (ΔΨ
    MeSH term(s) Animals ; Cells, Cultured ; Energy Metabolism/physiology ; Membrane Potential, Mitochondrial/physiology ; Mice ; Mitophagy/physiology ; Neurons/metabolism ; Protein Kinases/metabolism
    Chemical Substances Protein Kinases (EC 2.7.-) ; PTEN-induced putative kinase (EC 2.7.11.1)
    Language English
    Publishing date 2019-02-12
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80158-6
    ISSN 1471-4159 ; 0022-3042 ; 1474-1644
    ISSN (online) 1471-4159
    ISSN 0022-3042 ; 1474-1644
    DOI 10.1111/jnc.14667
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  10. Article ; Online: Peering into the ‘black box’ of pathogen recognition by cellular autophagy systems

    Shu-chin Lai / Rodney J Devenish

    Microbial Cell, Vol 2, Iss 9, Pp 322-

    2015  Volume 328

    Abstract: Autophagy is an intracellular process that plays an important role in protecting eukaryotic cells and maintaining intracellular homeostasis. Pathogens, including bacteria and viruses, that enter cells can signal induction of selective autophagy resulting ...

    Abstract Autophagy is an intracellular process that plays an important role in protecting eukaryotic cells and maintaining intracellular homeostasis. Pathogens, including bacteria and viruses, that enter cells can signal induction of selective autophagy resulting in degradation of the pathogen in the autolysosome. Under such circumstances, the specific recognition and targeting of the invading pathogen becomes a crucial step for the subsequent initiation of selective autophagosome formation. However, the nature of the signal(s) on the pathogen surface and the identity of host molecule(s) that presumably bind the signal molecules remain relatively poorly characterized. In this review we summarise the available evidence regarding the specific recognition of invading pathogens by which they are targeted into host autophagy pathways.
    Keywords autophagy ; E3 ligase ; galectin-8 ; tripartite motif proteins ; ubiquitin ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2015-08-01T00:00:00Z
    Publisher Shared Science Publishers OG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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