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  1. Book ; Online ; E-Book: Biochemistry and cell biology of ageing / Part 2

    Harris, J. Robin / Korolchuk, Viktor I.

    (Subcellular biochemistry ; 91)

    2019  

    Author's details J. Robin Harris, Viktor I. Korolchuk editors
    Series title Subcellular biochemistry ; 91
    Biochemistry and cell biology of ageing
    Collection Biochemistry and cell biology of ageing
    Language English
    Size 1 Online-Ressource (x, 499 Seiten), Illustrationen, Diagramme
    Publishing country Singapore
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    HBZ-ID HT020032369
    ISBN 978-981-13-3681-2 ; 9789811336805 ; 981-13-3681-4 ; 9811336806
    DOI 10.1007/978-981-13-3681-2
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Book ; Online ; E-Book: Biochemistry and cell biology of ageing / Part 1

    Harris, J. Robin / Korolchuk, Viktor I.

    (Subcellular biochemistry ; 90)

    2018  

    Author's details J. Robin Harris, Viktor I. Korolchuk editors
    Series title Subcellular biochemistry ; 90
    Biochemistry and cell biology of ageing
    Collection Biochemistry and cell biology of ageing
    Language English
    Size 1 Online-Ressource (x, 526 Seiten), Illustrationen, Diagramme
    Publishing country Singapore
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    HBZ-ID HT020032358
    ISBN 978-981-13-2835-0 ; 9789811328343 ; 981-13-2835-8 ; 981132834X
    DOI 10.1007/978-981-13-2835-0
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

    Full text online

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  3. Book ; Online: Biochemistry and cell biology of ageing

    Harris, J. Robin / Korolchuk, Viktor I.

    (Subcellular biochemistry)

    2018  

    Author's details J. Robin Harris, Viktor I. Korolchuk editors
    Series title Subcellular biochemistry
    Language English
    Dates of publication 2018-2019
    Publisher Springer
    Publishing place Singapore
    Publishing country Singapore
    Document type Book ; Online
    HBZ-ID HT020032346
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  4. Book ; Online ; E-Book: Biochemistry and cell biology of ageing / Part 4

    Harris, James R. / Korolchuk, Viktor I. / Harris, J. Robin

    (Subcellular biochemistry ; 103)

    2023  

    Author's details J. Robin Harris, Viktor I. Korolchuk editors
    Series title Subcellular biochemistry ; 103
    Biochemistry and cell biology of ageing
    Collection Biochemistry and cell biology of ageing
    Language English
    Size 1 Online-Ressource (viii, 458 Seiten), Illustrationen
    Publishing country Singapore
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    HBZ-ID HT030010407
    ISBN 978-3-031-26576-1 ; 9783031265754 ; 3-031-26576-9 ; 3031265750
    DOI 10.1007/978-3-031-26576-1
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

    Full text online

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  5. Book ; Online ; E-Book: Biochemistry and cell biology of ageing / Part 3

    Harris, James R. / Korolchuk, Victor I. / Harris, J. Robin / Korolchuk, Viktor I.

    (Subcellular biochemistry ; 102)

    2023  

    Author's details J. Robin Harris, Viktor I. Korolchuk editors
    Series title Subcellular biochemistry ; 102
    Biochemistry and cell biology of ageing
    Collection Biochemistry and cell biology of ageing
    Keywords Aging ; Cytology ; Clinical biochemistry ; Proteins
    Language English
    Size 1 Online-Ressource (ix, 424 Seiten)
    Publishing country Singapore
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    HBZ-ID HT021700279
    ISBN 978-3-031-21410-3 ; 9783031214097 ; 3-031-21410-2 ; 3031214099
    DOI 10.1007/978-3-031-21410-3
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

    Full text online

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  6. Article ; Online: Metabolic function of autophagy is essential for cell survival.

    Sedlackova, Lucia / Kataura, Tetsushi / Sarkar, Sovan / Korolchuk, Viktor I

    Autophagy

    2023  Volume 19, Issue 8, Page(s) 2395–2397

    Abstract: Age-related human pathologies present with a multitude of molecular and metabolic phenotypes, which individually or synergistically contribute to tissue degeneration. However, current lack of understanding of the interdependence of these molecular ... ...

    Abstract Age-related human pathologies present with a multitude of molecular and metabolic phenotypes, which individually or synergistically contribute to tissue degeneration. However, current lack of understanding of the interdependence of these molecular pathologies limits the potential range of existing therapeutic intervention strategies. In our study, we set out to understand the chain of molecular events, which underlie the loss of cellular viability in macroautophagy/autophagy deficiency associated with aging and age-related disease. We discover a novel axis linking autophagy, a cellular waste disposal pathway, and a metabolite, nicotinamide adenine dinucleotide (NAD). The axis connects multiple organelles, molecules and stress response pathways mediating cellular demise when autophagy becomes dysfunctional. By elucidating the steps on the path from efficient mitochondrial recycling to NAD maintenance and ultimately cell viability, we highlight targets potentially receptive to therapeutic interventions in a range of genetic and age-related diseases associated with autophagy dysfunction.
    MeSH term(s) Humans ; Cell Survival ; Autophagy ; NAD/metabolism ; Mitochondria/metabolism ; Aging/metabolism ; Poly(ADP-ribose) Polymerases/metabolism
    Chemical Substances NAD (0U46U6E8UK) ; Poly(ADP-ribose) Polymerases (EC 2.4.2.30)
    Language English
    Publishing date 2023-02-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2023.2165753
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6741: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: The evolution of selective autophagy as a mechanism of oxidative stress response: The evolutionarily acquired ability of selective autophagy receptors to respond to oxidative stress is beneficial for human longevity.

    Ratliffe, Joshua / Kataura, Tetsushi / Otten, Elsje G / Korolchuk, Viktor I

    BioEssays : news and reviews in molecular, cellular and developmental biology

    2023  Volume 45, Issue 11, Page(s) e2300076

    Abstract: Ageing is associated with a decline in autophagy and elevated reactive oxygen species (ROS), which can breach the capacity of antioxidant systems. Resulting oxidative stress can cause further cellular damage, including DNA breaks and protein misfolding. ... ...

    Abstract Ageing is associated with a decline in autophagy and elevated reactive oxygen species (ROS), which can breach the capacity of antioxidant systems. Resulting oxidative stress can cause further cellular damage, including DNA breaks and protein misfolding. This poses a challenge for longevous organisms, including humans. In this review, we hypothesise that in the course of human evolution selective autophagy receptors (SARs) acquired the ability to sense and respond to localised oxidative stress. We posit that in the vicinity of protein aggregates and dysfunctional mitochondria oxidation of key cysteine residues in SARs induces their oligomerisation which initiates autophagy. The degradation of damaged cellular components thus could reduce ROS production and restore redox homeostasis. This evolutionarily acquired function of SARs may represent one of the biological adaptations that contributed to longer lifespan. Inversely, loss of this mechanism can lead to age-related diseases associated with impaired autophagy and oxidative stress.
    Language English
    Publishing date 2023-08-21
    Publishing country United States
    Document type Journal Article
    ZDB-ID 50140-2
    ISSN 1521-1878 ; 0265-9247
    ISSN (online) 1521-1878
    ISSN 0265-9247
    DOI 10.1002/bies.202300076
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2024: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  8. Article ; Online: The crosstalk of NAD, ROS and autophagy in cellular health and ageing.

    Sedlackova, Lucia / Korolchuk, Viktor I

    Biogerontology

    2020  Volume 21, Issue 3, Page(s) 381–397

    Abstract: Cellular adaptation to various types of stress requires a complex network of steps that altogether lead to reconstitution of redox balance, degradation of damaged macromolecules and restoration of cellular metabolism. Advances in our understanding of the ...

    Abstract Cellular adaptation to various types of stress requires a complex network of steps that altogether lead to reconstitution of redox balance, degradation of damaged macromolecules and restoration of cellular metabolism. Advances in our understanding of the interplay between cellular signalling and signal translation paint a complex picture of multi-layered paths of regulation. In this review we explore the link between cellular adaptation to metabolic and oxidative stresses by activation of autophagy, a crucial cellular catabolic pathway. Metabolic stress can lead to changes in the redox state of nicotinamide adenine dinucleotide (NAD), a co-factor in a variety of enzymatic reactions and thus trigger autophagy that acts to sequester intracellular components for recycling to support cellular growth. Likewise, autophagy is activated by oxidative stress to selectively recycle damaged macromolecules and organelles and thus maintain cellular viability. Multiple proteins that help regulate or execute autophagy are targets of post-translational modifications (PTMs) that have an effect on their localization, binding affinity or enzymatic activity. These PTMs include acetylation, a reversible enzymatic modification of a protein's lysine residues, and oxidation, a set of reversible and irreversible modifications by free radicals. Here we highlight the latest findings and outstanding questions on the interplay of autophagy with metabolic stress, presenting as changes in NAD levels, and oxidative stress, with a focus on autophagy proteins that are regulated by both, oxidation and acetylation. We further explore the relevance of this multi-layered signalling to healthy human ageing and their potential role in human disease.
    MeSH term(s) Aging ; Autophagy ; Humans ; NAD ; Oxidation-Reduction ; Oxidative Stress ; Reactive Oxygen Species
    Chemical Substances Reactive Oxygen Species ; NAD (0U46U6E8UK)
    Language English
    Publishing date 2020-03-03
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2047160-9
    ISSN 1573-6768 ; 1389-5729
    ISSN (online) 1573-6768
    ISSN 1389-5729
    DOI 10.1007/s10522-020-09864-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5706: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  9. Article ; Online: The evolution of selective autophagy as a mechanism of oxidative stress response: The evolutionarily acquired ability of selective autophagy receptors to respond to oxidative stress is beneficial for human longevity

    Ratliffe, Joshua / Kataura, Tetsushi / Otten, Elsje G. / Korolchuk, Viktor I.

    BioEssays. 2023 Nov., v. 45, no. 11 p.e2300076-

    2023  

    Abstract: Ageing is associated with a decline in autophagy and elevated reactive oxygen species (ROS), which can breach the capacity of antioxidant systems. Resulting oxidative stress can cause further cellular damage, including DNA breaks and protein misfolding. ... ...

    Abstract Ageing is associated with a decline in autophagy and elevated reactive oxygen species (ROS), which can breach the capacity of antioxidant systems. Resulting oxidative stress can cause further cellular damage, including DNA breaks and protein misfolding. This poses a challenge for longevous organisms, including humans. In this review, we hypothesise that in the course of human evolution selective autophagy receptors (SARs) acquired the ability to sense and respond to localised oxidative stress. We posit that in the vicinity of protein aggregates and dysfunctional mitochondria oxidation of key cysteine residues in SARs induces their oligomerisation which initiates autophagy. The degradation of damaged cellular components thus could reduce ROS production and restore redox homeostasis. This evolutionarily acquired function of SARs may represent one of the biological adaptations that contributed to longer lifespan. Inversely, loss of this mechanism can lead to age‐related diseases associated with impaired autophagy and oxidative stress.
    Keywords DNA ; autophagy ; cysteine ; evolution ; homeostasis ; humans ; longevity ; mitochondria ; oligomerization ; oxidation ; oxidative stress ; protein folding ; reactive oxygen species ; stress response
    Language English
    Dates of publication 2023-11
    Publishing place John Wiley & Sons, Ltd
    Document type Article ; Online
    Note JOURNAL ARTICLE
    ZDB-ID 50140-2
    ISSN 1521-1878 ; 0265-9247
    ISSN (online) 1521-1878
    ISSN 0265-9247
    DOI 10.1002/bies.202300076
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

    Z 2009/501: Show issues

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  10. Article: Autophagy: 'Self-Eating' Your Way to Longevity.

    Pattison, Charlotte J / Korolchuk, Viktor I

    Sub-cellular biochemistry

    2019  Volume 90, Page(s) 25–47

    Abstract: Ageing is the gradual decline in biological function both at the cellular and organismal level. One of the key characteristics of cellular ageing is the accumulation of damaged proteins and organelles which, in turn, can cause cellular toxicity and death. ...

    Abstract Ageing is the gradual decline in biological function both at the cellular and organismal level. One of the key characteristics of cellular ageing is the accumulation of damaged proteins and organelles which, in turn, can cause cellular toxicity and death. Autophagy is an evolutionarily conserved process that is responsible for the sequestration of damaged or surplus cytoplasmic components which are then delivered to the lysosome for degradation. This house-keeping mechanism is essential to maintain cellular homeostasis and survival, particularly during stress. A decline or loss of sensitivity/responsiveness of autophagy is intimately linked with an accelerated rate of ageing as well as many age-related diseases including neurodegeneration, cancer and metabolic disease where damage accumulation exceeds damage removal. This chapter summarises current knowledge regarding the relationship between autophagy and ageing and outlines some strategies that can be implemented to promote the anti-ageing effects of autophagy to improve human health and lifespan.
    MeSH term(s) Autophagy ; Cellular Senescence ; Homeostasis ; Humans ; Longevity ; Lysosomes
    Language English
    Publishing date 2019-02-18
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 0306-0225 ; 0096-8757
    ISSN 0306-0225 ; 0096-8757
    DOI 10.1007/978-981-13-2835-0_2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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