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  1. Article: Deubiquitinating Enzymes in Parkinson's Disease.

    Chakraborty, Joy / Ziviani, Elena

    Frontiers in physiology

    2020  Volume 11, Page(s) 535

    Abstract: Mitochondrial dysfunction and neurodegeneration have been directly correlated in many neurodegenerative disorders. Parkinson's disease (PD) in particular has been extensively studied in this context because of its well-characterized association with ... ...

    Abstract Mitochondrial dysfunction and neurodegeneration have been directly correlated in many neurodegenerative disorders. Parkinson's disease (PD) in particular has been extensively studied in this context because of its well-characterized association with mitophagy, a selective type of autophagy that degrades mitochondria. Mitophagy is triggered by ubiquitin modification of proteins residing on the surface of mitochondria. Therefore, mitophagy is subject to suppression by deubiquitination. In recent years, many deubiquitinase enzymes (DUBs) emerged as therapeutic targets to compensate hindered mitophagy in PD. It is reasonable that inhibition of specific DUBs should induce mitophagy by blocking deubiquitination of mitochondrial proteins, although the signaling pathway is not always that linear. The broad aspect suggests that there could be cross talks among DUBs, which may in turn have synergistic effect to rescue the disease progression. In this short review we have highlighted DUBs that hold therapeutic value in the field of neurodegenerative diseases, PD in particular.
    Language English
    Publishing date 2020-06-03
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2020.00535
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Investigating mitochondrial autophagy by routine transmission electron microscopy: Seeing is believing?

    Chakraborty, Joy / Caicci, Federico / Roy, Moumita / Ziviani, Elena

    Pharmacological research

    2020  Volume 160, Page(s) 105097

    Abstract: Mitochondrial autophagy is affected in many diseases. In the past few years, the multiple-steps process of selective degradation of mitochondria has been dissected in details by combining outcomes from different approaches. Perhaps one of the most ... ...

    Abstract Mitochondrial autophagy is affected in many diseases. In the past few years, the multiple-steps process of selective degradation of mitochondria has been dissected in details by combining outcomes from different approaches. Perhaps one of the most rigorous methods to clearly visualise mitochondria undergoing autophagic engulfment and degradation, is transmission electron microscopy (TEM). In this opinion paper, we want to give a brief summary of the mitophagic process, and by which means mitophagy can be addressed, including TEM analysis. We will report examples of autophagy and mitophagy-related TEM images, and discuss how to decipher the different steps of the mitophagic process by routine TEM. In our opinion, this technique can be used as a powerful confirmatory approach for mitochondrial autophagy and can provide details of the organelle fate throughout the course of mitophagy with no substantial sample manipulation.
    MeSH term(s) Animals ; Humans ; Lysosomes/ultrastructure ; Microscopy, Electron, Transmission ; Mitochondria/ultrastructure ; Mitophagy ; Time Factors
    Language English
    Publishing date 2020-07-30
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1003347-6
    ISSN 1096-1186 ; 0031-6989 ; 1043-6618
    ISSN (online) 1096-1186
    ISSN 0031-6989 ; 1043-6618
    DOI 10.1016/j.phrs.2020.105097
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 721: Show issues Location:
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  3. Article ; Online: A trio has turned into a quartet: DJ-1 interacts with the IP3R-Grp75-VDAC complex to control ER-mitochondria interaction.

    Basso, Valentina / Marchesan, Elena / Ziviani, Elena

    Cell calcium

    2020  Volume 87, Page(s) 102186

    Abstract: The outer mitochondrial membrane protein VDAC interacts with the ER protein IP3R via chaperone Grp75 to form a molecular complex that couples mitochondria to the ER and contributes to functional mitochondria-ER contacts (MERCs), essential for efficient ... ...

    Abstract The outer mitochondrial membrane protein VDAC interacts with the ER protein IP3R via chaperone Grp75 to form a molecular complex that couples mitochondria to the ER and contributes to functional mitochondria-ER contacts (MERCs), essential for efficient calcium (Ca
    MeSH term(s) Endoplasmic Reticulum/metabolism ; HSP70 Heat-Shock Proteins/metabolism ; Humans ; Inositol 1,4,5-Trisphosphate Receptors/metabolism ; Membrane Proteins/metabolism ; Mitochondria/metabolism ; Protein Binding ; Protein Deglycase DJ-1/metabolism ; Voltage-Dependent Anion Channel 1/metabolism
    Chemical Substances HSP70 Heat-Shock Proteins ; Inositol 1,4,5-Trisphosphate Receptors ; Membrane Proteins ; glucose-regulated proteins ; Voltage-Dependent Anion Channel 1 (EC 1.6.-) ; Protein Deglycase DJ-1 (EC 3.1.2.-)
    Language English
    Publishing date 2020-02-24
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 757687-0
    ISSN 1532-1991 ; 0143-4160
    ISSN (online) 1532-1991
    ISSN 0143-4160
    DOI 10.1016/j.ceca.2020.102186
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Mitochondrial autophagy in the sleeping brain.

    Mauri, Sofia / Favaro, Mariavittoria / Bernardo, Greta / Mazzotta, Gabriella M / Ziviani, Elena

    Frontiers in cell and developmental biology

    2022  Volume 10, Page(s) 956394

    Abstract: A significant percentage of the mitochondrial mass is replaced on a daily basis via mechanisms of mitochondrial quality control. Through mitophagy (a selective type of autophagy that promotes mitochondrial proteostasis) cells keep a healthy pool of ... ...

    Abstract A significant percentage of the mitochondrial mass is replaced on a daily basis via mechanisms of mitochondrial quality control. Through mitophagy (a selective type of autophagy that promotes mitochondrial proteostasis) cells keep a healthy pool of mitochondria, and prevent oxidative stress and inflammation. Furthermore, mitophagy helps adapting to the metabolic demand of the cells, which changes on a daily basis. Core components of the mitophagy process are PINK1 and Parkin, which mutations are linked to Parkinson's Disease. The crucial role of PINK1/Parkin pathway during stress-induced mitophagy has been extensively studied
    Language English
    Publishing date 2022-08-24
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2022.956394
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Cell biology: The organelle replication connection.

    Ziviani, Elena / Scorrano, Luca

    Nature

    2016  Volume 538, Issue 7625, Page(s) 326–327

    MeSH term(s) DNA Replication ; Organelles
    Language English
    Publishing date 2016--20
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/538326b
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MO 244: Show issues

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  6. Article ; Online: Mitochondrial quality control beyond PINK1/Parkin.

    von Stockum, Sophia / Marchesan, Elena / Ziviani, Elena

    Oncotarget

    2018  Volume 9, Issue 16, Page(s) 12550–12551

    Language English
    Publishing date 2018-01-02
    Publishing country United States
    Document type Editorial
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.23799
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Boosting mitochondrial health to counteract neurodegeneration.

    Burtscher, Johannes / Romani, Mario / Bernardo, Greta / Popa, Traian / Ziviani, Elena / Hummel, Friedhelm C / Sorrentino, Vincenzo / Millet, Grégoire P

    Progress in neurobiology

    2022  Volume 215, Page(s) 102289

    Abstract: Mitochondrial health is based on a delicate balance of specific mitochondrial functions (e.g. metabolism, signaling, dynamics) that are impaired in neurodegenerative diseases. Rescuing mitochondrial function by selectively targeting mitochondrial ... ...

    Abstract Mitochondrial health is based on a delicate balance of specific mitochondrial functions (e.g. metabolism, signaling, dynamics) that are impaired in neurodegenerative diseases. Rescuing mitochondrial function by selectively targeting mitochondrial stressors, such as reactive oxygen species, inflammation or proteotoxic insults ("bottom-up" approaches) thus is a widely investigated therapeutic strategy. While successful in preclinical studies, these approaches have largely failed to show clear clinical benefits. Promoting the capacity of mitochondria - and other cellular components - to restore a healthy cellular environment is a promising complementary or alternative approach. Herein, we provide a non-technical overview for neurologists and scientists interested in brain metabolism on neuroprotective strategies targeting mitochondria and focus on top-down interventions such as metabolic modulators, exercise, dietary restriction, brain stimulation and conditioning. We highlight general conceptual differences to bottom-up approaches and provide hypotheses on how these mechanistically comparatively poorly characterized top-down therapies may work, discussing notably mitochondrial stress responses and mitohormesis.
    MeSH term(s) Exercise/physiology ; Humans ; Mitochondria/metabolism ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/therapy ; Neuroprotection ; Reactive Oxygen Species/metabolism
    Chemical Substances Reactive Oxygen Species
    Language English
    Publishing date 2022-05-28
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 185535-9
    ISSN 1873-5118 ; 0301-0082
    ISSN (online) 1873-5118
    ISSN 0301-0082
    DOI 10.1016/j.pneurobio.2022.102289
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  8. Article ; Online: Correction: Human frataxin, the Friedreich ataxia deficient protein, interacts with mitochondrial respiratory chain.

    Doni, Davide / Cavion, Federica / Bortolus, Marco / Baschiera, Elisa / Muccioli, Silvia / Tombesi, Giulia / d'Ettorre, Federica / Ottaviani, Daniele / Marchesan, Elena / Leanza, Luigi / Greggio, Elisa / Ziviani, Elena / Russo, Antonella / Bellin, Milena / Sartori, Geppo / Carbonera, Donatella / Salviati, Leonardo / Costantini, Paola

    Cell death & disease

    2024  Volume 15, Issue 1, Page(s) 93

    Language English
    Publishing date 2024-01-29
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-024-06459-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Activation of Ca

    Marchesan, Elena / Nardin, Alice / Mauri, Sofia / Bernardo, Greta / Chander, Vivek / Di Paola, Simone / Chinellato, Monica / von Stockum, Sophia / Chakraborty, Joy / Herkenne, Stephanie / Basso, Valentina / Schrepfer, Emilie / Marin, Oriano / Cendron, Laura / Medina, Diego L / Scorrano, Luca / Ziviani, Elena

    Cell death and differentiation

    2024  Volume 31, Issue 2, Page(s) 217–238

    Abstract: Selective removal of dysfunctional mitochondria via autophagy is crucial for the maintenance of cellular homeostasis. This event is initiated by the translocation of the E3 ubiquitin ligase Parkin to damaged mitochondria, and it requires the Serine/ ... ...

    Abstract Selective removal of dysfunctional mitochondria via autophagy is crucial for the maintenance of cellular homeostasis. This event is initiated by the translocation of the E3 ubiquitin ligase Parkin to damaged mitochondria, and it requires the Serine/Threonine-protein kinase PINK1. In a coordinated set of events, PINK1 operates upstream of Parkin in a linear pathway that leads to the phosphorylation of Parkin, Ubiquitin, and Parkin mitochondrial substrates, to promote ubiquitination of outer mitochondrial membrane proteins. Ubiquitin-decorated mitochondria are selectively recruiting autophagy receptors, which are required to terminate the organelle via autophagy. In this work, we show a previously uncharacterized molecular pathway that correlates the activation of the Ca
    MeSH term(s) Animals ; Calcineurin/metabolism ; Protein Kinases/genetics ; Protein Kinases/metabolism ; Phosphoric Monoester Hydrolases/metabolism ; Mitophagy/genetics ; Mitochondria/metabolism ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitin/metabolism ; Drosophila/metabolism ; Protein Serine-Threonine Kinases/metabolism ; Drosophila Proteins/genetics ; Drosophila Proteins/metabolism
    Chemical Substances Calcineurin (EC 3.1.3.16) ; Protein Kinases (EC 2.7.-) ; Phosphoric Monoester Hydrolases (EC 3.1.3.2) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Ubiquitin ; PINK1 protein, Drosophila (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Drosophila Proteins
    Language English
    Publishing date 2024-01-18
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1225672-9
    ISSN 1476-5403 ; 1350-9047
    ISSN (online) 1476-5403
    ISSN 1350-9047
    DOI 10.1038/s41418-023-01251-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MG 80: Show issues

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  10. Article ; Online: USP8 Down-Regulation Promotes Parkin-Independent Mitophagy in the

    Mauri, Sofia / Bernardo, Greta / Martinez, Aitor / Favaro, Mariavittoria / Trevisan, Marta / Cobraiville, Gael / Fillet, Marianne / Caicci, Federico / Whitworth, Alexander J / Ziviani, Elena

    Cells

    2023  Volume 12, Issue 8

    Abstract: Stress-induced mitophagy, a tightly regulated process that targets dysfunctional mitochondria for autophagy-dependent degradation, mainly relies on two proteins, PINK1 and Parkin, which genes are mutated in some forms of familiar Parkinson's Disease (PD). ...

    Abstract Stress-induced mitophagy, a tightly regulated process that targets dysfunctional mitochondria for autophagy-dependent degradation, mainly relies on two proteins, PINK1 and Parkin, which genes are mutated in some forms of familiar Parkinson's Disease (PD). Upon mitochondrial damage, the protein kinase PINK1 accumulates on the organelle surface where it controls the recruitment of the E3-ubiquitin ligase Parkin. On mitochondria, Parkin ubiquitinates a subset of mitochondrial-resident proteins located on the outer mitochondrial membrane, leading to the recruitment of downstream cytosolic autophagic adaptors and subsequent autophagosome formation. Importantly, PINK1/Parkin-independent mitophagy pathways also exist that can be counteracted by specific deubiquitinating enzymes (DUBs). Down-regulation of these specific DUBs can presumably enhance basal mitophagy and be beneficial in models in which the accumulation of defective mitochondria is implicated. Among these DUBs, USP8 is an interesting target because of its role in the endosomal pathway and autophagy and its beneficial effects, when inhibited, in models of neurodegeneration. Based on this, we evaluated autophagy and mitophagy levels when USP8 activity is altered. We used genetic approaches in
    MeSH term(s) Animals ; Humans ; Mitophagy/genetics ; Down-Regulation ; Drosophila/metabolism ; Drosophila melanogaster/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Protein Kinases/metabolism ; Brain/metabolism ; Neurons/metabolism ; Endopeptidases/metabolism ; Ubiquitin Thiolesterase/metabolism ; Endosomal Sorting Complexes Required for Transport/metabolism ; Protein Serine-Threonine Kinases/metabolism ; Drosophila Proteins/metabolism
    Chemical Substances Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Protein Kinases (EC 2.7.-) ; USP8 protein, human (EC 3.4.19.12) ; Endopeptidases (EC 3.4.-) ; Ubiquitin Thiolesterase (EC 3.4.19.12) ; Endosomal Sorting Complexes Required for Transport ; PINK1 protein, Drosophila (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Drosophila Proteins
    Language English
    Publishing date 2023-04-13
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells12081143
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