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  1. Article ; Online: RHIMoving fibrils of death.

    Tummers, Bart

    Cell research

    2023  Volume 33, Issue 11, Page(s) 811–812

    Language English
    Publishing date 2023-09-13
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 1319303-x
    ISSN 1748-7838 ; 1001-0602
    ISSN (online) 1748-7838
    ISSN 1001-0602
    DOI 10.1038/s41422-023-00875-3
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  2. Article: Editorial: Cell death: from its induction to the removal of dying cells!

    Tanzer, Maria C / Tummers, Bart / Poon, Ivan K H

    Frontiers in cell and developmental biology

    2023  Volume 11, Page(s) 1195775

    Language English
    Publishing date 2023-04-11
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2023.1195775
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  3. Article ; Online: Mechanisms of TNF-independent RIPK3-mediated cell death.

    Tummers, Bart / Green, Douglas R

    The Biochemical journal

    2022  Volume 479, Issue 19, Page(s) 2049–2062

    Abstract: Apoptosis and necroptosis regulate many aspects of organismal biology and are involved in various human diseases. TNF is well known to induce both of these forms of cell death and the underlying mechanisms have been elaborately described. However, cells ... ...

    Abstract Apoptosis and necroptosis regulate many aspects of organismal biology and are involved in various human diseases. TNF is well known to induce both of these forms of cell death and the underlying mechanisms have been elaborately described. However, cells can also engage apoptosis and necroptosis through TNF-independent mechanisms, involving, for example, activation of the pattern recognition receptors Toll-like receptor (TLR)-3 and -4, or zDNA-binding protein 1 (ZBP1). In this context, cell death signaling depends on the presence of receptor-interacting serine/threonine protein kinase 3 (RIPK3). Whereas RIPK3 is required for TNF-induced necroptosis, it mediates both apoptosis and necroptosis upon TLR3/4 and ZBP1 engagement. Here, we review the intricate mechanisms by which TNF-independent cell death is regulated by RIPK3.
    MeSH term(s) Apoptosis ; Cell Death ; Humans ; Receptor-Interacting Protein Serine-Threonine Kinases/genetics ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Serine ; Threonine ; Toll-Like Receptor 3/genetics
    Chemical Substances Toll-Like Receptor 3 ; Threonine (2ZD004190S) ; Serine (452VLY9402) ; RIPK3 protein, human (EC 2.7.11.1) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2022-10-18
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2969-5
    ISSN 1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
    ISSN (online) 1470-8728
    ISSN 0006-2936 ; 0306-3275 ; 0264-6021
    DOI 10.1042/BCJ20210724
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  4. Article ; Online: The evolution of regulated cell death pathways in animals and their evasion by pathogens.

    Tummers, Bart / Green, Douglas R

    Physiological reviews

    2021  Volume 102, Issue 1, Page(s) 411–454

    Abstract: The coevolution of host-pathogen interactions underlies many human physiological traits associated with protection from or susceptibility to infections. Among the mechanisms that animals utilize to control infections are the regulated cell death pathways ...

    Abstract The coevolution of host-pathogen interactions underlies many human physiological traits associated with protection from or susceptibility to infections. Among the mechanisms that animals utilize to control infections are the regulated cell death pathways of pyroptosis, apoptosis, and necroptosis. Over the course of evolution these pathways have become intricate and complex, coevolving with microbes that infect animal hosts. Microbes, in turn, have evolved strategies to interfere with the pathways of regulated cell death to avoid eradication by the host. Here, we present an overview of the mechanisms of regulated cell death in Animalia and the strategies devised by pathogens to interfere with these processes. We review the molecular pathways of regulated cell death, their roles in infection, and how they are perturbed by viruses and bacteria, providing insights into the coevolution of host-pathogen interactions and cell death pathways.
    MeSH term(s) Animals ; Cell Death/physiology ; Host-Pathogen Interactions/physiology ; Humans ; Necroptosis/physiology ; Pyroptosis/physiology ; Regulated Cell Death/physiology ; Signal Transduction/physiology
    Language English
    Publishing date 2021-09-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 209902-0
    ISSN 1522-1210 ; 0031-9333
    ISSN (online) 1522-1210
    ISSN 0031-9333
    DOI 10.1152/physrev.00002.2021
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  5. Article ; Online: Editorial

    Maria C. Tanzer / Bart Tummers / Ivan K. H. Poon

    Frontiers in Cell and Developmental Biology, Vol

    Cell death: from its induction to the removal of dying cells!

    2023  Volume 11

    Keywords efferocytosis ; cell death ; inflammation ; macrophages ; cytokines ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2023-04-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
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  6. Article ; Online: RIPped for neuroinflammation.

    Tummers, Bart / Green, Douglas R

    Cell research

    2017  Volume 27, Issue 8, Page(s) 1074

    Language English
    Publishing date 2017-08-01
    Publishing country England
    Document type Journal Article ; Published Erratum
    ZDB-ID 1319303-x
    ISSN 1748-7838 ; 1001-0602
    ISSN (online) 1748-7838
    ISSN 1001-0602
    DOI 10.1038/cr.2017.97
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  7. Article ; Online: Generation of

    Pelletier, Stephane / Tummers, Bart / Green, Douglas R

    STAR protocols

    2020  Volume 1, Issue 3, Page(s) 100181

    Abstract: The purpose of this protocol is to describe the generation of missense mutations in mice using CRISPR-Cas9 technology. The current protocol focuses on the generation of ... ...

    Abstract The purpose of this protocol is to describe the generation of missense mutations in mice using CRISPR-Cas9 technology. The current protocol focuses on the generation of a
    MeSH term(s) Alleles ; Animals ; Base Sequence ; CRISPR-Associated Protein 9/genetics ; CRISPR-Associated Protein 9/metabolism ; CRISPR-Cas Systems/genetics ; Caspase 8/genetics ; Female ; Genotype ; Mice, Inbred C57BL ; Mice, Transgenic ; Microinjections ; Polymerase Chain Reaction ; RNA, Guide, CRISPR-Cas Systems/genetics ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Recombinant Proteins/metabolism ; Zygote/metabolism
    Chemical Substances RNA, Guide, CRISPR-Cas Systems ; RNA, Messenger ; Recombinant Proteins ; CRISPR-Associated Protein 9 (EC 3.1.-) ; Caspase 8 (EC 3.4.22.-)
    Language English
    Publishing date 2020-11-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2666-1667
    ISSN (online) 2666-1667
    DOI 10.1016/j.xpro.2020.100181
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  8. Article ; Online: RIPped for neuroinflammation.

    Tummers, Bart / Green, Douglas R

    Cell research

    2017  Volume 27, Issue 9, Page(s) 1081–1082

    Abstract: Activation of the receptor interacting serine/threonine kinase (RIPK) 3 mediates an inflammatory type of cell death called necroptosis; in addition, RIPK3 has necroptosis-independent roles in inflammation, although these are not well defined. In a recent ...

    Abstract Activation of the receptor interacting serine/threonine kinase (RIPK) 3 mediates an inflammatory type of cell death called necroptosis; in addition, RIPK3 has necroptosis-independent roles in inflammation, although these are not well defined. In a recent study published in Cell, Daniels and colleagues demonstrate that RIPK3 controls West Nile virus infection by promoting neuroinflammation in the central nervous system without affecting neuronal death.
    MeSH term(s) Apoptosis ; Cell Death ; Central Nervous System ; Humans ; Inflammation ; Necrosis ; Receptor-Interacting Protein Serine-Threonine Kinases
    Chemical Substances RIPK3 protein, human (EC 2.7.11.1) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2017-05-19
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 1319303-x
    ISSN 1748-7838 ; 1001-0602
    ISSN (online) 1748-7838
    ISSN 1001-0602
    DOI 10.1038/cr.2017.75
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  9. Article ; Online: Generation of Casp8FL122/123GG Mice Using CRISPR-Cas9 Technology

    Stephane Pelletier / Bart Tummers / Douglas R. Green

    STAR Protocols, Vol 1, Iss 3, Pp 100181- (2020)

    2020  

    Abstract: ... on the use and execution of this protocol, please refer to Tummers et al. (2020). ...

    Abstract Summary: The purpose of this protocol is to describe the generation of missense mutations in mice using CRISPR-Cas9 technology. The current protocol focuses on the generation of a Casp8FL122/123GG missense mutation, but it can be adapted to introduce any missense or nonsense mutation.For complete details on the use and execution of this protocol, please refer to Tummers et al. (2020).
    Keywords Model Organisms ; CRISPR ; Science (General) ; Q1-390
    Language English
    Publishing date 2020-12-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
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  10. Article ; Online: Caspase-8: regulating life and death.

    Tummers, Bart / Green, Douglas R

    Immunological reviews

    2017  Volume 277, Issue 1, Page(s) 76–89

    Abstract: Roles for cell death in development, homeostasis, and the control of infections and cancer have long been recognized. Although excessive cell damage results in passive necrosis, cells can be triggered to engage molecular programs that result in cell ... ...

    Abstract Roles for cell death in development, homeostasis, and the control of infections and cancer have long been recognized. Although excessive cell damage results in passive necrosis, cells can be triggered to engage molecular programs that result in cell death. Such triggers include cellular stress, oncogenic signals that engage tumor suppressor mechanisms, pathogen insults, and immune mechanisms. The best-known forms of programmed cell death are apoptosis and a recently recognized regulated necrosis termed necroptosis. Of the two best understood pathways of apoptosis, the extrinsic and intrinsic (mitochondrial) pathways, the former is induced by the ligation of death receptors, a subset of the TNF receptor (TNFR) superfamily. Ligation of these death receptors can also induce necroptosis. The extrinsic apoptosis and necroptosis pathways regulate each other and their balance determines whether cells live. Integral in the regulation and initiation of death receptor-mediated activation of programmed cell death is the aspartate-specific cysteine protease (caspase)-8. This review describes the role of caspase-8 in the initiation of extrinsic apoptosis execution and the mechanism by which caspase-8 inhibits necroptosis. The importance of caspase-8 in the development and homeostasis and the way that dysfunctional caspase-8 may contribute to the development of malignancies in mice and humans are also explored.
    Language English
    Publishing date 2017-05
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 391796-4
    ISSN 1600-065X ; 0105-2896
    ISSN (online) 1600-065X
    ISSN 0105-2896
    DOI 10.1111/imr.12541
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